Focused cardiac ultrasound (FCU) can be used in veterinary patients. In the acute care setting, FCU provides useful information to help diagnose and treat patients that present in states of extremis. Importantly, current veterinary FCU is restricted to basic assessment of the morphology of the heart and provides significantly less information compared to a comprehensive echocardiogram performed by a cardiologist. The field of veterinary critical care echocardiography—advanced bedside echocardiography for assessment and decision making in intensive care patients—is in its infancy; FCU should be used cautiously in decision making in the intensive care patient that has already received fluids, medications, and life-supporting interventions.

The learning objectives of this lecture are:

• Describe a systematic approach to focussed cardiac ultrasound.
• Appreciate the role of focused cardiac ultrasound for patients presenting in shock.
• Understand the limitations of focused cardiac ultrasound.

FCU Views

Focused cardiac ultrasound is intended to be quick and easy to perform. As such, we use views that are familiar and relatively easy to acquire.

Three main views exist:

• Right parasternal short axis (PSAX) at the level of the papillary muscles (the ‘mushroom view’).
• Right parasternal short axis (PSAX) at the level of the heart base (the ‘LA:Ao view’).
• Right parasternal long axis (PLAX) four chamber view, which includes the two ventricles and the two atria.

Other views can be useful, though require additional time to acquire and/or to master:

• Subxiphoid (transdiaphragmatic)
• Right parasternal short axis at the level of the mitral valve.
• Right parasternal long axis five chamber view, which includes the aorta.

Left sided and apical views are achievable, though require significant expertise and are typically not included in basic FCU protocols.

FCU and Shock Classification

There are three ways to use FCU to investigate shock in the acute patient.

1. Classification by Shock Pathophysiology

There are four major classes of cardiovascular shock: hypovolaemic vs. obstructive vs. maldistributive vs. cardiogenic. Using FCU to classify shock this way is quick, easy, and logical; it is an example of a pattern recognition approach. This approach starts at the end and works backward, i.e., you already suspect the type of shock and, perhaps subconsciously, try to fit the FCU findings to affirm your suspicions. This might work with, for example, a dog with haemoperitoneum and a small left ventricle—i.e., hypovolaemic shock—or pericardial effusion—i.e., obstructive shock. However, it is less useful for complex situations, where multiple processes are occurring concurrently, which may not fit nicely into one class.

2. Classification by Heart Type

This approach starts differently, though remains an example of pattern recognition. Using FCU, a quick idea of the apparent phenotype of the heart is obtained, e.g., ‘it looks like hypertrophic cardiomyopathy’ in a cat. This approach works on the principle of simplicity: what you see is likely what is happening, or at least is contributing to the patient’s clinical status. History and physical examination improve this approach, e.g., an older cat with a gallop rhythm and pleural effusion, with a heart that looks hypertrophic. It assumes that the apparent phenotype explains the clinical presentation and defines the type of shock. It is prone to over and under-inference (we see things that are not there and we miss things that are there). Its usefulness is limited in complex situations.

3. Systematic Classification

Individual regions are systematically assessed and their structural appearance described. A very basic assessment of function is obtained. The FCU description of the heart is then integrated with the clinical presentation. This approach is expected to improve detection of abnormalities, particularly in complex situations, providing a better understanding of the current structure and function of the heart. This should improve communication, particularly with the cardiology service. It separates the heart from the disease, which is not clinically accurate, so it is essential to integrate the FCU findings with the clinical findings. Importantly, it accepts that FCU does not solely define shock. Developing a systematic FCU approach is a step towards formalizing veterinary critical care echocardiography.

A systematic approach will be discussed below. It is presented as four steps. The FCU does not need to be performed perfectly in order, with each step isolated from the others. For example, assessing fluid tolerance (step four) can be ongoing throughout FCU.

Systematic Approach to FCU

1. Pericardial Effusion - Is There Pericardial Effusion?

Pericardial effusion (PCE) is the accumulation of excessive fluid within the pericardial sac. The first question of the systematic approach is ‘is there pericardial effusion?’ If the answer is no, move on to the next step. Pericardial effusion is easily identified by the right PSAX and PLAX views; if in doubt, a subxiphoid view can be useful. The main differentials for peri-cardiac fluid accumulations seen via FCU are an enlarged left atrium (LA) and pleural effusion. Due to the limited ultrasound sector size, an enlarged LA can appear as a large fluid accumulation: using multiple views can help differentiate LA enlargement from PCE. Pleural effusion can present a challenge: PCE tends to be ventrally dependent (collects preferentially around the apex) and can be differentiated using multiple views. Grading of PCE has been suggested (mild <1 cm, moderate 1–2 cm, marked >2 cm) with the implication that mild effusions are unlikely the cause of shock; however, this does not consider the rate of accumulation.

Cardiac tamponade occurs when fluid accumulating in the pericardial sac impedes cardiac filling. We frequently infer cardiac tamponade via a classic presentation of compromised perfusion (hypotension/syncope/collapse/poor pulses) + tachycardia + right atrial inversion. Right atrial (RA) inversion is not specific for tamponade in humans. Inversion occurs first at end diastole, when the atrioventricular valves are closed, and the RA pressure is at its lowest. Inversion that occurs >1/3 of the cardiac cycle is more specific for tamponade. This is very difficult to identify bedside with canine and feline heart rates. Thus, the longer the RA inversion, the more likely tamponade physiology exists. The pressure in the RV is higher than the RA; the RV pressure is lowest in early diastole; RV inversion tends to occur in early diastole when the atrioventricular valves are open. Right ventricular inversion is less sensitive and more specific for tamponade than RA inversion. Left atrial inversion is considered very specific for pericardial tamponade. Left ventricular inversion is unexpected: it is sometimes seen with regional PCE-tamponade in humans after interventional procedures. Other indicators of tamponade physiology include: pulsus paradoxicus (a decrease in systolic blood pressure by 10 mm Hg on inspiration, as a function of ventricular interdependence) and electrical alternans (beat-to-beat alterations in QRS complex). The caudal vena cava (CVC) can be evaluated by the subxiphoid view: if it is not dilated or there are good respiratory variations in diameter, reconsider tamponade physiology.

Caveats exist for PCE in veterinary medicine. Small breed dogs with PCE tend to have left atrial tears associated with mitral valve disease: Pericardiocentesis might not be advisable. In trauma, rapid accumulations can cause tamponade; pericardial thrombi might be seen and cannot be removed by pericardiocentesis. With chronic pulmonary hypertension, the right heart chambers might not invert due to pressure elevations; LA inversion may be seen.

2. The Right Heart (Specifically, the Right Ventricle)

The right heart is evaluated using the two right PSAX and the PLAX 4 chamber views; other views, such as the subxiphoid and the PLAX 5 chamber, can provide useful information. Slight adjustments can optimize the right heart views. Apical views are used in human critical care echocardiography, though they are difficult to acquire in veterinary species.

The geometry of the RV makes evaluation of systolic function difficult using FCU. We, therefore, rely on markers of right heart “health.” The right heart appearance can vary with haemodynamic status and with acute versus chronic diseases. Right heart abnormalities suggest that a patient will be a fluid non-responder, perhaps fluid intolerant. Right heart dysfunction can be associated with left ventricular (LV) underfilling and decreased cardiac output; it can simulate “fluid responsive” profiles, even with more advanced dynamic tests. Right heart changes are also important during positive pressure ventilation.

The RV:LV size ratio is typically 1:3. Above 1:2 suggests RV enlargement; 1:1 implies, with relatively high certainty, that the right heart is contributing to the current clinical status of the patient. Generally, the RV wall is half as thick as the LV. A thickened RV wall implies chronicity (adaptation). The absence of hypertrophy does not rule out a right heart problem, as acute processes can cause severe right heart compromise.

The interventricular septum is useful for FCU right heart assessment. Diastolic flattening of the right heart indicates volume overload. Pressure overload can result in septal flattening throughout the cardiac cycle. Either way, there is a right heart problem and the patient might be fluid intolerant. Using FCU we can only see the more extreme cases and we miss early or mild cases. In states of haemodynamic instability, moderate right heart compromise can sometimes seem less severe - this is a significant limitation of right heart FCU.

The CVC via the subxiphoid view is useful when considering the right heart. A dilated CVC that lacks respiratory-linked size variations suggests either volume status is OK, or the right heart cannot accommodate more fluids. The hepatic veins, which have less echogenic walls than the portal veins, can engorge in right heart diseases, similarly suggesting fluid intolerance. What if the right heart looks big but the CVC is highly collapsible? This situation is unclear and different methods should be used to assess the patient. Recently our group developed a 10-point FCU score for pulmonary hypertension in dogs. A score >5 is strongly indicative of pulmonary hypertension, providing the history and clinical findings are similarly consistent. A score ≤2 suggests pulmonary hypertension is not present. This scoring system assumes cardiac changes have occurred in a patient with pulmonary hypertension. The eccentricity index, which is the ratio of two orthogonal diameters of the LV, is a marker of LV deformation due to RV overload and has been investigated briefly.

3. The Left Heart (Specifically, the Left Ventricle)

Contraction of the left ventricle is complex, with longitudinal, radial, and circumferential deformations. Assessing LV function independent of loading conditions (preload, afterload) is difficult using FCU. It can be simplified, accepting significant limitations in our assessments. Qualitative assessment can be performed quickly and easily bedside and avoids measurement errors associated with quantitative assessment, which can lead to significant inaccuracies with FCU. Qualitative assessments can themselves be inaccurate, lack repeatability and have a tendency toward false findings (over and under-inference). Imaging the LV is easily achieved via the two right PSAX and the right PLAX 4 chamber views; care must be taken to avoid foreshortening of the ventricle. The right PLAX 5 chamber and subxiphoid views can be used. Apical views are useful, though perhaps not for FCU currently. Initial characterization: ‘is the LV function subjectively normal/hyperdynamic versus decreased?’ Eyeballing may be useful for overtly decreased systolic function, though in other scenarios is probably only accurate when performed by an experienced echocardiographer. Increased end systolic diameter (ESD) and end diastolic diameter (EDD) measurements can suggest decreased contractile function and ventricular dilation, respectively. These measurements are not independent of loading conditions. They are weak surrogates for ejection fraction: increased ESD and EDD can occur with normal ejection fraction. Image acquisition and measurement error can lead to false findings.

Various FCU techniques to assess segmental area change exist. Using orthogonal (right PSAX at the level of the papillary muscles and the right PLAX 4 chamber) views, an idea of LV contractile function can be obtained. The LV is divided vertically and horizontally into four segments in each view. Three questions are asked of each segment during contraction: 1) Is the lumen reducing (is the anechoic space becoming smaller)? 2) Is the LV wall moving centripetally? 3) Is the LV wall thickening? If the answer to any of these is ‘no’ in any segment, there is an LV problem. This technique improves the identification of regional LV abnormalities. Fractional shortening (FS%) is a quantitative method measured via right PSAX at the level of the papillary muscles, just below the mitral valve. Positioning is important: measurements too far apically or basally will give false results; the ventricle must be cut perpendicularly. Fractional shortening is limited by poor imaging quality, regional wall abnormalities, abnormal septal motion, and electrical conduction abnormalities. Smaller LVs tend toward higher FS%, larger LVs tend toward lower FS%: this does not reflect alterations in cardiac output. Significant breed variation exists. B-mode acquisition may be useful with FCU when alignment for M-mode is not possible. The accuracy and repeatability of fractional shortening measured via B-mode using FCU in emergency settings is unknown.

The normal/hyperdynamic heart: with hypovolaemia, the LV is typically small with obliteration of the lumen during systole (‘kissing ventricles’). History, physical examination (rectal examination) and point-of-care-ultrasound can confirm situations, such as haemorrhage. This patient is likely fluid responsive. Caution is advised with cats, as hypertrophic phenotype cardiomyopathy (HCM) can mimic these signs and normally indicates fluid intolerance: a LV wall thickness ≥6 mm cat supports the suspicion of HCM. In sepsis, hyperdynamic LV contractions are suggestive of high-output shock. This is a function of ventriculoarterial coupling. With hypotension + normal LV diastolic area + LV collapse during systole, we can infer decreased afterload. In septic humans, LV and RV dysfunction is estimated to occur in 70% and 30%, respectively. Vasopressors can unmask systolic dysfunction, as increasing afterload alters ventriculoarterial coupling. Hyperdynamic contractions can also be seen with mitral regurgitation: alternative outflow into the LA can be considered to decrease afterload. Whereas septic patients might benefit from fluids, patients with significant mitral regurgitation are likely fluid intolerant. Breed, history, and LA enlargement can assist in identifying significant mitral regurgitation. Colour Doppler can also be helpful.

Diastology, the study of diastolic function, is currently not considered in FCU. As critical care echocardiography evolves, diastology is likely to become increasingly important.

4. The Fluid Intolerant Heart

Fluids are a mainstay of shock treatment. Predicting which patients may benefit from fluids (fluid responders) and which may experience a detrimental effect (fluid intolerant) is challenging. Focussed cardiac ultrasound highlights morphological features that are quicker and easy to identify; it does not sufficiently evaluate functional parameters. There are no FCU parameters that accurately and consistently predict fluid responsiveness.

Fluid tolerance describes the capacity to accept fluids without adverse effect. Tolerance is specific to each organ and each vascular bed. For example, it is conceivable to experience pulmonary endothelial damage, where fluid administration results in oedema, with concurrent increase in cardiac output if that patient is also preload responsive. Haemodynamic fluid intolerance can be evaluated via central venous pressure (CVP) and venous flow parameters, where an elevation in CVP or venous congestion (or flow reversal) suggest intolerance. Dynamic fluid intolerance occurs when a patient seems fluid tolerant considering venous parameters but fails to respond to a fluid bolus. This may be encountered with sepsis-induced vasodilation and concurrent myocardial depression. This has been demonstrated in humans where 1/4 patients with CVP <5 mm Hg and 1/5 patients with a collapsible inferior vena cava were fluid non-responders.

Though FCU may not provide specific commentary on cardiac function, it can provide relatively strong suggestions that a patient is a fluid non-responder, perhaps fluid intolerant. While not an absolute contraindication to fluid infusion, these findings oblige the clinician to think twice. Views include the two right PSAX views, the right PLAX four chamber view and the CVC. Apical views, though useful, are limited by their acquisition. Left atrial enlargement implies fluid intolerance. Subtle enlargement is difficult to appreciate, though an ‘absolutely massive’ LA indicates intolerance. Similarly, RA enlargement suggests intolerance. The atria should be roughly equal in size with a straight interatrial septum: bowing of the septum implies enlargement of the encroaching atrium and fluid intolerance.

Right ventricular failure results in underfilling of the LV, which can mistakenly be interpreted as hypovolaemia if the left heart is considered in isolation. Right heart pathologies strongly indicate that, if fluids are necessary, they should be given cautiously: rapid, high-volume boluses should be avoided. Early use of vasopressors and/or inotropes may be considered. Decreased LV systolic function suggests fluid intolerance. With concurrent b-lines on lung ultrasound, fluid intolerance should be assumed until proven otherwise. Breed and history are helpful (e.g., a Doberman with exercise intolerance). An empty LV, or systolic obliteration of the LV, is not specific for hypovolaemia—history and clinical exam findings should be integrated with FCU. A patient with hypertrophic-phenotype cardiomyopathy, which may present with decreased LV lumen diameters, is fluid intolerant unless there is good reason to believe otherwise.

Ejection fraction is often measured by cardiologists and is dependent on ventriculoarterial coupling (the balance between arterial elastance and LV end-systolic elastance). Changes in ejection fraction do not equate to fluid responsiveness; using FCU surrogates to comment on perceived ejection fraction does not equate to fluid responsiveness.

Inferior and superior vena cavae measurements have been investigated in humans. Data are also available for dogs. Assessment of the CVC is in vogue; however, there are significant limitations in the published data, acquisition of measurements and interpretation of results. In short, CVC measurements comment on the x-axis of the Frank-Starling curve, distinct from the y-axis. Caudal vena cava measurements assessed by FCU are subject to significant confirmation and desirability biases. A recent (2018) meta-analysis considering inferior vena cava static and dynamic measurements in humans concluded that they do not reliably predict fluid responsiveness (typically defined as an increase in cardiac output following a fluid challenge). ‘Extreme heterogeneity’ was reported amongst the studies included, which likely prevented a single meaningful conclusion from the batched data. Vena cava measurements may be useful in specific cases, particularly when combined with a comprehensive clinical assessment. Currently, a dilated/fat caudal vena cava, which lacks respiratory variations, in a dog, suggests that this patient is unlikely to respond to a fluid bolus: by extrapolation, fluids may be harmful.

Challenges When Interpreting FCU Findings

Arrhythmias and tachycardias complicate FCU interpretation. In human medicine, rates over 120 beats per minute are often described as problematic: these rates are common in shocked veterinary patients. Concurrent ECG may be useful but adds time and complexity. The heart that looks small (e.g., with reduced LV diameters), in a patient that is ambulatory can be confusing. A small heart in isolation does not necessitate fluid therapy; however, some patients (e.g., a dog with pre-crisis hypoadrenocorticism) may indeed have a decreased total body fluid status.

Changes to FCU findings should not be expected to occur following an intervention (e.g., fluid bolus). Focused cardiac ultrasound is mostly a tool to assess morphological appearance, not functional response. This emphasises that FCU is not a target itself, rather it is a descriptive tool. That said, overt changes are often seen with vasoactive medications. Vasopressor administration can unmask occult systolic dysfunction, though FCU is unable to quantify true systolic dysfunction versus iatrogenic changes to ventriculoarterial coupling.

The septic patient with pre-existing cardiac disease presents a challenge. Normally, patients with structural heart diseases (e.g., mitral valve disease, dilated cardiomyopathy) are considered fluid intolerant. However, studies in human medicine suggest that fluid loading in septic patients with pre-existing heart failure is not detrimental and perhaps advantageous. A similar situation might be envisaged in a dog with pre-existing systolic dysfunction and acute gastric dilation-volvulus.

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