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Newsletter dmd1.2.9.html

Determining the Basic Haemodynamic state using focussed Echocardiography

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By Alistair Royse and Colin Royse

Clinical Professor of Medicine, University of Melbourne
Director of Diploma of Perioperative and Critical Care Echocardiography

Sections
Summary
Example
Haemodynamic state assessment
7 Basic haemodynamic states
4 Assessment steps to determing the basic haemodynamic state
Step 1: Estimate volume
Step 2: Estimate systolic function
Step 3: Estimate left atrial pressure
Step 4: Final assessment
Influending management
Other findings Valves, RAP, RVSP, CO
Abbreviations
Resources
Videos
Disclaimer and Copyright

Summary
In all forms of critical care medicine there may be significant derrangements from the normal haemodynamic state.  Even in the best equipped metropolitan trauma centres with the most sophisticated invasive monitoring equipment, it is still difficult to accurately diagnose the underlying Basic Haemodynamic state.  Without this knowledge, therapeutic interventions to correct the haemodynamic abnormality are likely to be flawed.  Little wonder therefore that these problems are magnified in smaller settings or, in the case of the military, surgical facilities with basic equipment only.  In the case of military personnel being treated, generally it is assumed (reasonably) that the patients are young and fit with normal underlying ventricular function.  However, increasingly in military conflicts these facilities are also engaged in treating civilian casualties from the general population where age and other comorbidities including cardiac disease may be present, to confound the diagnosis and management of haemodynamic instability.

Echocardiography is superior to invasive pressure monitoring because it may directly measure ventricular volume, function and provides for a more accurate estimate of the left atrial pressure state.  The integration and these three parameters allows one to more accurately determine the correct underlying Basic Haemodynamic state.

Philosophically, it is better for the treating physician to assess the haemodynamic state themselves, and in real time, in order to guide immediate and real-time changes to therapy.  To the extent that the treating physician delegates the diagnostic element to a third-party surrogate or third-party service there may be a delay; and perhaps a full comprehensive assessment performed which takes more time than is required to determine the key element of the diagnosis of haemodynamic state. This degrades the notion of real-time monitoring assessment guiding real-time immediate changes to therapy.  Therefore, ideally those medical specialties not currently trained in the technologies of ultrasound, or echocardiography should consider learning to use these technologies (perhaps in a limited fashion), to allow for rapid and real-time diagnosis guiding immediate and real-time changes to therapy; and then reassessment shortly after instituting changes to therapy to further guide fine tuning to the therapy.  We have called this HEARTscan (haemodynamic echocardiography assessment in real time).

Military trauma example
Consider a soldier and a 60-year-old civilian casualty arriving acutely following a blast injury from an improvised explosive device.  Let us say both had identical injuries with 15% burns to the legs and lower abdomen, some blast injury to the lungs with pneumothorax requiring intercostal catheter placement and ventilation. Also  surgical debridement of some abdominal wounds including a bowel injury.  24 hours later, 10 units of blood and 12 L of crystalloid or colloid fluids have been administered yet both patients remain hypotensive and oliguric.  The central venous pressure is 3 mmHg.  In the case of the young soldier, the issues relate to hypovolaemia from third space losses, volume loss from the burns, vasodilation from sepsis and reduced venous return from positive pressure ventilation.  Echocardiography here could determine the accurate haemodynamic state by determining the left atrial pressure state which, if low, would suggest volume was required; and if normal it would suggest vasoconstrictors were required.  The more elderly gentleman however could easily have underlying ischaemic cardiac disease, diastolic dysfunction from any cause or even valvular pathologies.  Echocardiography could detect all of these accurately even when performed in a limited fashion to the extent that it may influence the key therapeutic choices.  In other words, in the critically ill following trauma, the most common finding from invasive pressure monitoring is of low systemic arterial blood pressure and low right atrial pressure.  In the young this does not differentiate between a vasodilated state and hypovolaemia; and in the older population it cannot additionally easily differentiate between primary diastolic failure, systolic failure, diastolic and systolic failure or indeed some valvular pathologies.  Surprisingly, ultrasound-based technologies are relatively easy to learn when used in a limited fashion for purposes such as determining the basic haemodynamic state.

Haemodynamic state assessment
The abnormal haemodynamic state is often first noted by a change in blood pressure, heart rate or some other evidence of poor tissue perfusion such as a cold or cyanosis of the periphery, reduced urine output or metabolic acidosis.  However, even with invasive pressure monitoring, it is difficult to determine whether the cause of the haemodynamic abnormality is due to changes in volume or ventricular function.  Even with advanced monitoring system such as thermodilution Swan-Ganz pulmonary artery catheter, there is significant guesswork often required in determining the underlying haemodynamic abnormality.  The reason is the pressure based assessment of myocardial function does not provide accurate assessment of ventricular volume.  For example, a high pulmonary artery wedge pressure (PCWP) in the setting of low cardiac output (CO) and hypotension could be caused by any of the following - (1) left ventricular systolic failure, (2) right ventricular failure or (3) left ventricular diastolic failure.

This point is illustrated by the following example:-
A 70-year-old man, escaping from his burning house, falls and fractures his hip.  At surgery, his blood pressure is 140/90 mmHg, but within 10 minutes of the commencement of his anaesthetic, his blood pressure falls to 85/50 mmHg.  His heart rate remains unchanged at 70 beats per minute.  A vasoconstrictor is administered which increases the blood pressure for 5 minutes only.  A central venous catheter is then placed and his right atrial pressure is elevated at 10 mmHg, indicating an abnormal haemodynamic state and that he is unlikely to be hypovolaemic.  However it is not useful in determining the precise haemodynamic state present which may be either systolic or diastolic left ventricular failure (or both), vasodilation or right ventricular failure.  A pulmonary artery Swan-Ganz catheter is inserted and his cardiac index was found to be low at 1.9 L/min/m2 , and the pulmonary capillary wedge pressure is elevated at 17 mmHg.  These findings would suggest vasodilation is unlikely, but it cannot further differentiate between diastolic or systolic left ventricular failure, or indeed right ventricular failure.  The correct therapy is different for each of these possibilities.  However these can be accurately determined using echocardiography as described below.

There are seven basic haemodynamic states:-

1.  Normal
2.  Empty (hypovolaemic)
3.  Primary diastolic failure
4.  Primary systolic failure
5.  Systolic and diastolic failure
6.  Vasodilation
7.  Right ventricular failure

There are four assessment steps to determine the basic haemodynamic state:-

1.  Estimate volume
2.  Estimate systolic function
3.  Estimate filling pressure
4.  Final assessment (interpreting the results).

Step 1: Estimate volume
This reflects estimation of left ventricular end-diastolic volume (Preload). Unlike non-invasive monitoring, echocardiography can directly measure ventricular volume.  Two-dimensional echocardiography measures the area in one plane, and from this information volume is estimated.  Transthoracic echocardiography may view the left ventricle in long axis from the parasternal long axis view (PLAX), but generally it is easier to appreciate volume from cross-sectional view of the left ventricle which is obtained from the parasternal short axis view (PSAX).  With practice, the observer may note pattern recognition of normal or abnormal states even without specific measurement.  A useful tip is to set depth of the ultrasound probe to the same value initially (usually 16 cm), which will provide a standardised cardiac size.  Consequently, a ventricle that is dilated, or hypovolaemic (empty) can be immediately recognized even before specific measurement made, See Figure 1

Figure 1.  Estimate left ventricular volume (PLAX).
Fig1
                                Empty   (see video)                                                  Normal        (see video)                                                          Dilated (see video)

 

Table 1. Assessment of systolic function.

Table1

Step 2: Estimate systolic function
Systolic function can be empirically appreciated best in the PSAX view.  Estimates of ejection fraction (EF) can be calculated from calculating the fractional shortening (FS), Figure 2, which measures the change in left ventricular diameter between systole and diastole measured at the base of the mitral valve leaflets and is usually performed the PLAX view.  The ejection fraction can also be estimated by calculating the fractional area change of the left ventricle between systole and diastole as measured at the mid papillary level of the left ventricle.  This method is more common with transoesophageal echocardiography than transthoracic echocardiography.  Table 1 shows the numeric value ranges for both of these measurements.  Systolic function is estimated as Normal, Increased or Reduced.

Figure 2. M-mode measurement of ventricle.

Fig2
                                                           

Step 3: Estimate left atrial pressure
The step is most important to be able to differentiate the presence or absence of diastolic left ventricular dysfunction.  Primarily left atrial pressure (LAP) is categorised into Normal or High, but it is of some additional use to be able to categorise it as Low to be able to identify a hypovolaemic state.  Echocardiography assessment of left atrial pressure however is reasonably reliable for qualitative assessment but relatively poor for quantitative assessment.  Fortunately, quantitative assessment is not particularly important for determining the basic haemodynamic state assessment because we are primarily interested in identifying whether the left atrial pressure state is

Figure 3. Estimate left atrial pressure by interatrial septum motion.
TTE PSAX, Apical 4 chamber views.
(see video section)

Figure3

high or normal.  In approximate terms, high LAP would be equivalent to a pulmonary capillary wedge pressure (PCWP) > 15 mmHg.  There are numerous methods or techniques described for estimating left atrial pressure, but the following two examples are recommended:-

Shape and movement of the interatrial septum
Normally, the interatrial septum (IAS) moves towards the right atrium for most of the cardiac cycle; but during mid systole, there is a transient reversal where the interatrial septum bows towards the left atrium, see Figure 3.  This motion is reflected of the relative differences in pressure between the right atrium and the left atrium over time. With a high LAP, the pressure of the left atrium exceeds the pressure of the right atrium at all times, and so the interatrial septum bows towards the right atrium throughout the cardiac cycle.  When the patient is being ventilated, this motion is further accentuated. During the inhalation phase of ventilation, the interatrial septal motion towards the right atrium is further exaggerated, but with normal LAP, the interatrial septum will go towards the left atrium during exhalation.  However, the septum will remain fixed and bowed towards the right atrium during inhalation and exhalation in the setting of a raised LAP.  Conversely, when the patient is hypovolaemic and the atria are relatively empty, then there is exaggerated motion of the interatrial septum in both directions throughout the cardiac cycle.  Commonly, the interatrial septum appears redundant, and the central portion will form folds (concertina or buckling), and this reflects a low LAP.

The interatrial septum can be viewed from the PSAX view where the aortic valve is seen in cross-section, and the interatrial septum arises from the non coronary cusp, Figure 3.  Also, the interatrial septum can be seen well from the apical 4 chamber view.

Systolic vs. diastolic components of the pulmonary vein flow
One of the pulmonary veins is imaged, and pulsed wave Doppler is used to interrogate the flow.  Normal LAP is characterised by a proportion of flow in systole (S wave) exceeding the proportion of flow in diastole (D wave) - S>D, see Figure 4.  The full description is beyond the scope of this paper, however in a high LAP S < D.

Figure 4. Estimate left atrial pressure by pulmonary vein Doppler.

Fig4

Step 4: Final assessment (Interpretation)
The key difference between echocardiography and invasive pressure monitoring assessment is that echocardiography can directly assess ventricular volume, systolic function and filling pressure.  This combination of knowledge allows us to estimate preload, ventricular function and importantly, ventricular compliance (diastolic function).  Only when we can estimate ventricular compliance and volume together, are we able to differentiate diastolic heart failure from other haemodynamic states.

See Table 2 as a guide to the interpretation.  In trauma and sepsis, the most common differentiation is between hypovolaemia (empty) and a vasodilated state.  In the more elderly population superadded diastolic ventricular dysfunction is an important consideration; or in the trauma setting where there may have been a chest injury resulting in some myocardial injury.  Yet the most difficult haemodynamic state to understand and to diagnose is primary diastolic dysfunction.  This is because the left ventricle appears to be hypovolaemic (empty), yet also appears to have normal systolic function.  Therefore, the initial impression is that the patient is hypovolaemic, but in hypovolaemia there is a low LAP.  In primary diastolic failure, there is a high LAP, yet there is inadequate filling of the left ventricle because it is poorly compliant (stiff).  Clearly assessment of the left atrial pressure state and integrating this with the volume assessment allows us to infer that compliance of the left ventricle.

Table 2. Interpretation of the findings

Table2

Using Table 2 to interpret your findings:-
1.  Normal haemodynamic state.  This is characterised by normal volume, normal systolic function and normal LAP.
2.  Empty (hypovolaemic).  This is characterised by reduced volume, normal or increased systolic left ventricular function and low LAP.
3.  Primary diastolic failure.  The ventricle will appear hypovolaemic (reduced volume), it will have normal systolic function - but high LAP.  This is the most difficult haemodynamic state to appreciate because it looks normal.  It requires a conceptual leap to believe that the normal looking ventricle actually constitute heart failure.  The key to identifying this state is to see a normal looking ventricle operating at high LAP.
4.  Primary systolic failure.  This is characterised by an increased volume (dilated left ventricle), reduced systolic function and normal LAP.  This means that the compliance of the left ventricle (diastolic function) is normal or even increased.  This form of heart failure is far easier to manage by the use of inotropes than one with superadded diastolic dysfunction.
5.  Systolic and diastolic failure.  In this haemodynamic state, there is increased left ventricular volume, reduced systolic function and high LAP.  These patients represent the most severe form of heart failure and the most difficult to manage since inotropes will generally address the systolic failure alone without altering the diastolic failure.  Commonly there is also associated right ventricular failure as well.
6.  Vasodilation. This is characterised as by normal left ventricular volume and normal LAP, but increased systolic function. This hyperdynamic left ventricular function is a result of reduced systemic vascular resistance and therefore there is augmented systolic ejection. A visual clue is where the papillary muscles touch at the end of systole – the “kissing” sign.
7.  Right ventricular failure.  This is characterised by a dilated right ventricle with reduced inward excursion of the free wall and high LAP.  Although isolated right ventricular failure may occur (e.g. major pulmonary embolism), it is frequently associated with left ventricular failure and mitral valve regurgitation.  It may also contribute to left ventricular diastolic dysfunction by the compressing the interventricular septum and therefore contributing to reduced ventricular compliance as evidenced by a high LAP.

Influencing management according to the Basic Haemodynamic state
The first principle of real-time echocardiography assessment to determine the haemodynamic state is that it is performed at the time of management intervention (in real time).  This is a derivation of our acronym for the limited echocardiography course HEARTscan ( Haemodynamic Echocardiography Assessment in Real Time) which is meant to illustrate that this imaging modality is used as a sophisticated real-time haemodynamic monitor which will then guide immediate alterations to haemodynamic management. 

The second principle is that a correct diagnosis is made for the underlying basic haemodynamic state, and echocardiography has an advantage over any form of invasive pressure monitoring assessment since it may directly assess ventricular volume, function and left atrial pressure state. 

The final principle relates to the correct choice of treatment for the relevant haemodynamic state.  It is most important to understand that echocardiography assessment of the haemodynamic state is much more important than the clinical signs and symptoms of the patient, since several abnormal haemodynamic states may have identical signs and symptoms (and indeed may have very similar pressure monitoring parameter measurements). This final point is crucial since it remains a frequent occurrence that there are widely varying opinions regarding the correct treatment for various haemodynamic states (e.g. treating a vasodilated state with additional intravenous volume loading, rather than the use of vasoconstrictors; or the treatment of primary diastolic failure with inotropes that had little effect on diastolic function).

See Table 3 for a suggested therapeutic approach for each haemodynamic state. The management of systolic left ventricular failure is straightforward and responds well to the inotrope therapy.  However, the treatment of diastolic failure is very different and problematic as there is no specific drug or agent that adequately corrects diastolic failure.  For example, use of an inodilator is a relatively common therapy for patients with dilated cardiomyopathy.  Logically, increasing systolic function thereby increasing ejection fraction should improve global myocardial performance.  The primary limitation in diastolic failure is that the stoke volume of the left ventricle is reduced, because of the reduced end diastolic volume (reduced left ventricular filling due to increased left ventricular stiffness); rather than reduced systolic function.  The use of an inodilator may in fact be counter-productive because it may reduce the preload to the heart is a consequence of venodilation or because of a tachycardia resulting in reduced filling time of the left ventricle as well as causing an increased injection fraction.  The management of hypovolaemia is volume replacement; however an acute increase in preload to the ventricle is possible with use of vasoconstrictors as this will also constrict venous

Table 3. Possible therapies for abnormal haemodynamic states.


Haemodynamic state

Possible therapies

Normal

No change

Empty

Intravenous volume

Primary diastolic failure

Maintain preload
Control heart rate
Treat coexisting vasodilation with vasopressor
Possible low dose inotrope to support right ventricular function

Primary systolic failure

Inotropes or inodilator

Systolic and diastolic failure

Inodilators
Consider pacing faster if available or chronotropic agents

Vasodilation

Vasoconstrictors (not volume loading)

Right ventricular failure

Inodilators
Treat coexisting vasodilation with vasopressor
Pulmonary artery dilators such as nitric oxide

capacitance vessels and therefore augment venous return to the heart.  Therefore, even in hypovolaemia the use of vasoconstrictors may be useful as a short-term measure until volume is able to be administered.  The treatment of a vasodilated state is the use of vasoconstrictors which will constrict both the arterial and venous system.  One of the primary failures of invasive pressure monitoring in a vasodilated state is the presence of low right atrial pressure which suggests to the observer hypovolaemia; yet there is no true hypovolaemia and the pressure is low due to dilation of the venous capacitance vessels.  Administering excessive amounts of volume intravenously may be counter-productive.  However, in critically ill patients such as burns, trauma or septic patients patients, it is possible that there is both vasodilation and relative hypovolaemia.  The key point to the management is to first correct the vasodilation with vasoconstrictors, and when relatively normal vascular resistance is achieved then additional intravenous volume can be administered as required.

Other findings


Valves
It is important to appreciate that a full interrogation of cardiac valves is well beyond the scope of knowledge and technique of a limited and focussed echocardiography study. However, it is easy to appreciate on 2-dimensional imaging, minor degrees of valvular thickening, restriction of leaflet motion or minor regurgitation on colour flow mapping, that could be categorised as “not clinically significant”. Conversely, gross valve leaflet thickening, restriction of leaflet motion or gross regurgitation is also easy to appreciate and categorised as “potentially clinically significant”. If there is doubt then this too would lead the clinician to consider it as potentially significant – which would then lead them to consider this abnormality as impacting on their treatment. (It would of course be mandatory that a referral for a subsequent comprehensive echocardiography study be made).

Estimate of right atrial pressure (RAP)
In the subcostal view, the inferior vena vaca (IVC) is imaged in longitudinal plane and if collapsed throughout most of the cardiac cycle if considered Low (< 5 mmHg). If it is not collapsed for most of the cardiac cycle but does collapse by 50% during inspiration then is Normal (5-10 mmHg); but if it dilated throughout all parts of the cardiac cycle and does not appear to collapse then the RAP is Elevated (>10 mmHg). Specific measurements or manoeuvres are beyond the scope of a limited focused study.

Estimate right ventricular systolic pressure (RVSP)
Sometimes, in the more elderly or difficult patients, an estimate of the pulmonary artery pressures is useful. If some tricuspid regurgitation is present, then continuous wave Doppler (CW) is placed through this regurgitant jet and the peak velocity measured. This estimated pressure is displayed by the machine, and equates to 4v2, where v = the peak velocity of the regurgitation jet. This value is added to RAP to estimate RVSP.

Cardiac output
Although a more advanced application, this too is easy to estimate. Usually the left ventricular outflow tract diameter is measured at the base of aortic valve and the cross sectional area calculated. A CW trace through the AV is then measured and the Doppler flow signal is traced yielding the distance along the trace called the velocity time integral (VTI).
CO = VTI x Area x heart rate.

Resources

HEARTscanTM                  
Haemodynamic Echocardiography Assessment in Real Time 
http://www.heartweb.com.au/training/HEARTscan.html

HEARTscan Report Form  (requires Adobe Acrobat 7 or later)
http://www.heartweb.com.au/dmd/d/HEARTscanRpt.pdf

Handbook of Perioperative and Critical Care Echocardiography from McGraw-Hill
http://www.heartweb.com.au/Publications/pocketguide.html

Videos
Streaming Flash video
htpp://www.heartweb.com.au/dmd/dmd1.2.9.html#videos

Parasternal Long axis (PLAX)
Empty
Normal
Dilated

Parasternal Short axis (PSAX)
Normal
Normal MP

Apical 4 Chamber (A4C)
Normal
Dilated poor LV
Dilated
Restrictive

Interatrial Septum motion (IAS)
Normal PSAX

Abbreviations

PLAX                       Parasternal long axis view of the heart (TTE)
PSAX                       Parasternal short axis view of the heart (TTE)
Apical 4 Chamber   View from the fifth intercostal space over the apex of the left ventricle with views of both atria and ventricles (TTE)
TTE                         Transthoracic echocardiography
TOE                         Transoesophageal echocardiography
TEE                          Transesophageal echocardiography
TG                           Transgastric view of TOE
PCWP                      Pulmonary capillary wedge pressure
CVP                         Central venous pressure
CO                          Cardiac output
CI                            Cardiac index (CO / body surface area)
PW                           Pulsed wave Doppler
CW                          Continous wave Doppler
S wave                    PW of pulmonary vein flow during systole
D wave                   PW of pulmonary vein flow during diastole
FS                            Fractional shortening
EF                            Ejection fraction
FAC                         Fractional area change
LAP                         Left atrial pressure
IAS                          Interatrial septum
AV                           Aortic valve
MV                          Mitral valve
RAP                         Right atrial pressure
RVSP                       Right ventricular systolic pressure
Diastolic dysfunction    Reduced left ventricular compliance (increased stiffness) resulting from poor relaxation during diastole

Disclaimer
The views of this paper reflect those of the author and do not reflect on any organisation or group. This Newsletter, does not seek to support any views or counter views expressed, but does seek to stimulate debate on controversial areas of medicine.

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