Cardiology Case #10
Primary Author: Dr Alastair Robertson; Co-Authors: Dr Hywel James and David Law
Background:
A 36 year old female was brought to ED by ambulance with severe breathlessness that had developed over an hour or so. She had a background of mild asthma with no prior ICU admissions.
Initial assessment demonstrated:
Agitated and diaphoretic patient, with decreased air entry throughout.
Initial Observations: RR 36, Sats 96% on 6L, HR 125, BP 110/70, temp 35.5
Chest XR showed hyper-inflated lungs with bilateral pulmonary infiltrates.
ECG is shown below, what do you think?
-
ECG shows a sinus tachycardia with a rate of 120/min. There is normal axis and intervals.
There is marked widespread ST depression and T-wave inversion, most obvious in the inferior and lateral leads.
Differential would include RV strain due to e.g. PE (although typically T wave changes are seen in V1-3), LV strain, myocardial ischaemia.
This ECG should be a prompt to assess for cardiac pathology.
Respiratory distress was initially thought to be obstructive airways disease +/- respiratory sepsis.
Venous blood gas showed:
pH 6.95, CO2 68, HCO3 14, Anion Gap 18, Lac 13
- - - > mixed metabolic and respiratory acidosis,
Managed initially with BiPAP, bronchodilators and antibiotics.
She deteriorated further and was subsequently intubated for ongoing respiratory failure despite escalation in management. CTPA was negative for PE.
Post-intubation she remained hypotensive despite a noradrenaline infusion.
Cardiac POCUS:
In the setting of undifferentiated shock, ultrasound can be key.
Below are the initial Parasternal long-axis and apical views.
What do you think is going on?
-
As always, the parasternal long-axis can give a key summary of cardiac function. This view is a “low” parasternal, close to the costal margin on the left (~3rd - 4th rib space) due to the lack of a true parasternal window in this patient.
The LV function is severely impaired suggesting a severe cardiomyopathy. There is some contraction at the LV base, but the mid-cavity and apex are severely impaired.
Of note there is no pericardial effusion excluding tamponade as a differential for shock.
The apical view confirms global LV dysfunction, particularly mid-LV and apex. The RV also has significantly impaired systolic function suggesting bi-ventricular failure.
This patient is in cardiogenic shock.
POCUS Pearls:
Assessing LV dysfunction
The views above show bi-ventricular failure, with poor LV function in particular. Myocardial ischaemia is a major differential so assessment of the LV looking for territorial movement abnormalities is important. Go back and review the ECG, the ST and T-wave changes are widespread, but more prominent inferiorly and laterally.
The A4C view shows widespread LV dysfunction with sparing of the base. Remember that in A4C the lateral wall is generally supplied by the Lcx, and the septum is generally supplied by the RCA (proximally), and then the LAD (apically).
Assessment of the Apical 2-chamber, and Long-axis was also useful:
In the A2C (video 1), the anterior (right side) wall and the apex is supplied by LAD. The inferior (left) wall is supplied (proximal 2/3) by the RCA usually.
In the Long-axis (video 2) the septum (right wall) is supplied by the LAD, whilst the posterior (left) or inferolateral wall is generally supplied by the LCx (though the proximal part may be RCA).
No clear territorial abnormalities were noted, the LV base appeared to have some contractility, but the entire mid-cavity and apex were akinetic.
It is worth noting that the density in the inferior apex was favoured to be trabeculation rather than mural thrombus, though these patients are at risk of apical thrombus.
Differentials:
When addressing an acute, severe cardiomyopathy such as this consider:
Ischaemic cardiomyopathy, especially LAD occlusion
Myocarditis:
Infective (viral, bacterial, fungal, parasites [Chagas disease])
Autoimmune
Drug-induced
Severe Takotsubo Cardiomyopathy
Drug induced (particularly stimulants, cocaine, other toxins)
Peripartum Cardiomyopathy (typically last month of pregnancy to 6-months postpartum)
Alcoholic Cardiomyopathy
Consider Septic Cardiomyopathy or Severe Acidosis as causes
Other: (Thiamine deficiency/Wet Beri-Beri, Hyperthyroid, other metabolic)
Intermediate POCUS:
Assessment of filling pressures and cardiac output
The stroke volume and LV filling pressures can be useful to guide inotropy and diuresis which are generally the mainstays of treatment for this condition.
In Case 8 (pericardial effusion) we introduced assessment of LVOT VTI to look for respiratory variation in flow out of the LV (echogenic “pulses paradoxus”).
LVOT VTI is measured by putting PW doppler in the LVOT, just proximal to the aortic valve in an apical 5-chamber view. The doppler signal should be a triangular signal, followed immediately by a spike which is the closing click of the aortic valve. The VTI is the area under that triangle (calculated by the machine after one traces around the triangle - see dotted line below)
The stroke volume can be calculated by multiplying the LVOT VTI by the area of the LVOT. The LVOT diameter is measured on PLAX, and is usually around 20-24mm, thus allowing the area to be calculated (A = π x rad squared)
However, in a time limited POCUS with critically unwell patients the VTI alone can be used as a rough measure of cardiac output (not forgetting that cardiac output will also depend on the heart rate, and the size of the LVOT).
A VTI of around 18-22cm is generally considered normal.
This still of PW doppler in the LVOT shows an LVOT VTI of 9.16cm which is significantly reduced confirming our diagnosis of cardiogenic shock.
Focus on Ejection Fraction:
This is important in ED to gauge severity of LV impairment, assess whether this is the primary cause for the patient’s symptoms, and if we need to intervene acutely (with e.g. inotropes).
LV systolic impairment can be segmental (e.g. in acute MI) or global (e.g. in myocarditis).
Ejection Fraction is a reasonable measure of impairment, and is generally graded as follows:
Hyperdynamic - >65%
Normal - 50-65%
Mild Impairment - 45-50%
Moderate Impairment 30-45%
Severe Impairment <30%
EF can be measured in several ways:
1) Visual Estimation (the ‘eyeball’ method): requires a lot of experience to accurately estimate EF qualitatively but gross function can be assessed rapidly. In cases such as this one could estimate the likelihood of severe impairment from eyeballing the images. Most believe a in novices qualitative approach underestimates true LVEF.
2) Linear Method/Fractional Shortening: Measures the LV cavity base, either still images or in M-mode (with cursor in the middle of the LV, not to include the papillary muscles or Mitral valve). The ‘Teichholz’ method measures in a parasternal long axis using a formula.
How? Use the freeze function, then scroll through the stills to measure the maximum LV diameter in end-diastole [LVEDD] (just as mitral valve closes), and then again in end-systole [LVESD]. Most machines will calculate the ‘fractional shortening’ of the LV, then use that to estimate an ejection fraction. Can also be done in PSAX +/- m-mode.
*Caveat the value does NOT express EF, since it’s a measure of distance not volume. Easy…..the US machine computes the EF by converting diameters into volumes using the aformetioned Teichholz equation.
As this method generally only measures the LV base, it can overestimate the EF in cases where basal motion is preserved but the apex is hypokinetic (e.g. takotsubo), and underestimate the EF if basal motion is impaired but the rest of the LV is functioning (e.g. posterior MI)
3) E-Point Septal Separation (EPSS): refers to distance between the anterior mitral valve leaflet (AMVL) and the septum, when the MV has reached maximum excursion during early diastolic filling.
- larger the EPSS distance = the worse the ejection fraction.
How? obtaining a good PSLAX view + horizontally-orientated LV. Place M-mode cursor over the tip of the AMVL as it moves towards the septum. In M-mode measure the distance between the MV “E-wave”.
EPSS <8mm = normal EF, 8-18mm Mild-Moderate reduced EF, >18mm severely reduced LVEF
EPSS in M-mode
4) 3D Echo / Simpson’s Biplane: This is the considered the most accurate method of calculating EF, but requires software which is generally only found on dedicated echo machines. It requires good quality images of the LV apically (ideally A4C and A2C) to be obtained, and software then analyses the LV in all 3-dimensions to calculate an overall volume change. The operator must be able to get good apical images, and then check that the software is tracking the LV walls faithfully for this method to work well.
For this patient - the visual estimation was of severe LV impairment with an EF of well under 30%
This was confirmed via the Linear Method, which estimated an EF of around 18% despite the fact that some basal motion was preserved.
On formal 3D echo the Simpson’s Biplane calculated the EF slightly higher at 25%. this was due to some preserved longitudinal contraction of the LV meaning that the base was moving upwards to reduce LV volume, which is movement that is missed by the linear method.
EPSS was not possible given the limited higher window for a PLAX.
All 3 methods applied confirmed a severely reduced EF
Case Conclusion
This patient was started on a dobutamine infusion in ED with the goal of improving cardiac contractility. She was continued on noradrenaline to maintain systemic vascular resistance, as dobutamine can cause some peripheral vasodilation due to beta-effect.
They responded well to dobutamine with an improvement in blood pressure and was stable on transfer to ICU, allowing some cautious diuresis. Gases gradually improved, and hsTroponin peaked at around 400. Serial echocardiograms showed steady improvement of cardiac function over the next few days. Coronary angiogram was delayed until post-extubation, and showed normal LV function and normal coronary arteries.
Likely diagnosis (of exclusion) was thought to be Takotsubo cardiomyopathy. This is an example of severe Takotsubo as the basal motion was impaired (rather than hyper dynamic) and the EF was significantly reduced.
POCUS Summary:
Use of POCUS can be critical in identifying cardiac pathology.
In this case the diagnosis shifted from respiratory +/- sepsis, to cardiac which required a different approach to management.
Try to learn to visually estimate EF. In cases of severe impairment (EF <30%) very close attention needs to be paid to volume status and cardiac function to manage these patients well in ED.
Before you go………..IVC Measurements
Bear in mind that IVC measurements to assess volume status may be unreliable in patients on mechanical ventilation or NIV.
In spontaneously ventilating patients a maximal IVC size of <2cm, and/or collapsibility of >50% on inspiration may be markers to suggest that the patient will be fluid-responsive (as part of a more comprehensive assessment).
In patients on positive-pressure ventilation, the IVC below the diaphragm may distend (rather than collapse) with inspiration (due to positive pressure compressing venous return in the thorax). A distention of >20% with inspiration may suggest an element of fluid-responsiveness, however this assessment is much more nuanced and IVC measurements alone should not be used to determine volume status, particularly in intubated patients.
We will aim to cover this in more detail in another case.
