Echocardiography in intensive care

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Chapter 23 Echocardiography in intensive care

Echocardiography refers to a group of interrelated ultrasound applications used to examine the heart and great vessels. The reflected and processed sonic waves are displayed on a monitor and the images can be stored on videotape or disk. Echocardiography includes: (1) two-dimensional (2-D) anatomical imaging; (2) M-mode echocardiography, usually obtained with 2-D guidance; and (3) Doppler techniques. Echocardiography is a safe non-invasive technique which is integral to clinical cardiology. More recently, echocardiography has evolved into a powerful diagnostic and management tool in critically ill patients, especially in cardiovascular emergencies of uncertain cause.1,2

Cardiologists, although highly skilled in echocardiography, may not appreciate the complex pathophysiology of critically ill patients in intensive care, and they have time commitments elsewhere. Echocardiography is operator-dependent; optimal image acquisition requires both technical knowledge of the machine’s capabilities as well as a degree of manual dexterity. As a general rule, echocardiography is not an efficient technique for monitoring haemodynamic indices over the medium term (hours–days) in the intensive care unit (ICU). Echocardiography can help determine whether and when continuous haemodynamic monitoring should be commenced.3 Repetitive trend measurements, such as stroke volume, cardiac output and pulmonary artery wedge pressure, are more suited to the pulmonary artery catheter. Moreover, intensive care staff are skilled and experienced in its use. Echocardiography technicians are not present in ICU, especially out of hours; intensivists must be able to act as their own sonographers as well as interpreting and reporting on the echographic images obtained. It is important that intensivists acquire all requisite skills so that echocardiography becomes more widely available.

PRINCIPLES AND TECHNICAL CONSIDERATIONS4

Echocardiography uses the reflection of sound waves at tissue boundaries to construct a 2-D image of cardiac structures. The human ear hears only sound waves with a frequency between 20 Hz and 20 kHz; higher frequencies are referred to as ultrasound. Echocardiography uses sound in the frequency 1–10 MHz. A piezo electrical crystal generates and receives the ultrasound waves.

2-D ECHOCARDIOGRAPHY

2-D echocardiography is the cornerstone of cardiac ultrasound as Doppler and M-mode are usually performed with reference to the 2-D image. Each 2-D image is defined by the position of the transducer (acoustic window) and image plane which is determined by the axis of the heart and not the spine (Table 23.1).

Table 23.1 Some standard views in transthoracic and transoesophageal echocardiography

Acoustic window Image plane
Transthoracic
Parasternal Long axis
  Short axis
Apical Four-chamber
  Two-chamber
  Long axis
Subcostal Multiple
Transoesophageal*
Transgastric e.g. Short axis
  Long axis
Deep transgastric e.g. Long axis/five-chamber
Lower transoesophageal e.g. Four-chamber
  Two-chamber
  Long axis
Upper transoesophageal e.g. Short axis of aortic valve
  Long axis of aortic valve
  Right ventricular inflow–outflow

* Multiple image planes from 0° to 180°.

DOPPLER ECHOCARDIOGRAPHY4,5

Doppler echocardiography is vital for obtaining haemodynamic information and is an integral part of every echocardiographic study.

The Doppler effect is based on changes in sound frequency that occur when a sound source moves towards or away from an observer. One classic example is that of an ambulance siren; as it comes toward a listener, the sound frequency increases (higher pitch) and after the ambulance moves away from the observer the sound frequency decreases (lower pitch).

The Doppler shift is the difference between frequencies that are transmitted and received by a transducer after striking red blood cells.

The Doppler equation is the mathematical relationship between the Doppler shift and the velocity of red blood cells that produce it.

image

where V = velocity of blood flow, C = speed of sound in soft tissue (1540 m/s), Δf = Doppler (frequency) shift:difference in frequency between received (fr) and transmitted (ft) ultrasound and θ = angle between ultrasound beam and direction of blood flow (Figure 23.2). Echocardiographic machines contain computers that automatically calculate the Doppler shift which is then entered into the Doppler equation. Blood flow velocity (m/s) is calculated and displayed on the monitor.

It is very important that the ultrasound beam is parallel or nearly parallel with the direction of blood flow. Ifθ equals 0 then cosign θ equals 1; however, if θ > 20° then the velocity of blood flow will be significantly underestimated. Doppler data are processed and a spectral display plots instantaneous blood velocities over time. Blood flow velocity can be expressed as peak velocity or mean velocity throughout a cardiac cycle (velocity–time integral: VTI) (Figure 23.3).

The most common uses of Doppler are pulsed-wave (PW), continuous-wave (CW) and colour-flow Doppler (CFD).

TRANSTHORACIC (TTE) AND TRANSOESOPHAGEAL ECHOCARDIOGRAPHY

TTE and TOE are complementary ultrasound techniques, each with its own strengths and weakness (Table 23.2). For example, a vegetation imaged on the mitral valve of a septic patient will usually require a TOE to evaluate complications of endocarditis.

INDICATIONS FOR ECHOCARDIOGRAPHY11,12

The indications for echocardiography broadly fall into three categories:

Guidelines for the use of echocardiography are based on expert consensus and observational studies. There are no randomised trials that specifically test the impact of echocardiography on outcome. In intensive care practice, echocardiography is used to evaluate clinical syndromes that suggest a diagnosis or, more often, a number of possible diagnoses. For example, haemodynamic instability in a patient with major blunt chest trauma suggests cardiac contusion or pericardial effusion causing tamponade. Nevertheless, the echocardiographic examination might reveal hypovolaemia with hyperdynamic LV systolic function or valvular damage with severe regurgitation.

Some common syndromes in which echocardiography is especially useful are listed in Table 23.3.

Table 23.3 Indications for echocardiography in the intensive care unit according to clinical syndrome

Clinical syndrome Findings Comments
Hypotension
Acute myocardial infarct    
No murmur LV RWMA(s) Usually severe ↓ LV systolic function
  RV RWMA RV ↓ > LV ↓
  Hypovolaemia ‘Empty’ LV cavity, systolic function largely preserved
  Acute MR Often no murmur with normal LA size
New murmur Papillary muscle rupture (partial or complete) ‘Good’ LV function with severe MR
  VSD RWMA. High-velocity left-to-right systolic jet
Rarely Cardiac rupture/tamponade Acute pericardial tamponade, usually fatal
  LV pseudoaneurysm Containment of rupture
Cardiothoracic surgery Cardiac tamponade Often localised. There may be no ‘echo-free space’ due to clot compressing the heart. Cardiac filling pressures may be normal
(New) RWMA May be due to graft occlusion, air embolism
Hypovolaemia ‘Empty’ LV with RWMA
Global LV ↓ Stunning or long-standing cardiomyopathy
Valvular dysfunction Often long-standing but may be worsened by surgery, e.g. ischaemia to a papillary muscle of mitral valve
Dynamic LVOT obstruction LVOT pressure gradient, SAM, MR Inotropes/IABP/hypovolaemia worsen LVOT obstruction
Trauma Hypovolaemia ‘Empty’ LV with vigorous contraction
Cardiac contusion RWMA (RV > LV)
Valvular injury Most common aortic valve (AR) or mitral valve (MR), occasionally tricuspid valve (TR)
VSD/ASD Occasionally
Cardiac tamponade More common in penetrating chest injuries
Ruptured thoracic aorta Widened mediastinum (90%) at isthmus of aorta. TOE required
Sepsis Often normal LV systolic function with ‘empty’ LV Possible global/regional LV depression
Infective endocarditis – vegetations/abscess/regurgitation TOE more sensitive than TTE for imaging vegetations/abscess/fistula
‘Isolated’ hypotension (‘hypotension ?cause’) Global LV ↓ or RWMA Cardiomyopathy or stunning
Valvular dysfunction Usually chronic, occasionally acute (e.g. ruptured papillary muscle of mitral valve)
Dynamic LVOT obstruction  
Acute cor pulmonale Pulmonary embolism – usually dilated right heart with depressed systolic function, sometimes with clot in a proximal pulmonary artery
Sepsis (source?) Vegetations, regurgitation ± abscess Infective endocarditis until proven otherwise
Normal TOE examination Infective endocarditis unlikely. If clinically indicated serial TOE
Systemic emboli (source?) LA/LAA clot Usually enlarged LA and atrial fibrillation TOE usually required for diagnosis
LV clot Usually associated with RWMA or global LV depression. TTE for apical clot
Aortic atherosclerotic TOE essential for diagnosis plaques
Vegetations – aortic or abscess Septic?
Clot – prosthetic aortic or mitral valve Associated prosthetic valve dysfunction
Patent foramen ovale with paradoxical embolism RA pressure > LA pressure (e.g. IPPV with high PEEP). TOE (bubble contrast) usually necessary for diagnosis
Tumour (e.g. LA myxoma) Uncommon
Pulmonary oedema (cause?) ↓ LV systolic/diastolic function Isolated LV diastolic dysfunction not uncommon
Valvular dysfunction (MR, MS, AR, AS) If flail leaflet/ruptured papillary muscle suspected then TOE indicated
Intracardiac shunt  
Normal Suggests non-cardiac cause (e.g. ARDS)
Dyspnoea/hypoxia without pulmonary oedema (dyspnoea cause?) Pulmonary embolism (dilated right heart chambers ± clot in pulmonary artery) Infers moderate to large clot burden i.e. submassive/massive PE
Cardiac tamponade Usually other clinical signs of tamponade present
Miscellaneous e.g. chronic cor pulmonale, RVH, constrictive pericarditis, diastolic dysfunction, intracardiac shunt, RV volume overload  
Chest pain of uncertain aetiology (chest pain cause?) RWMA Infers presence of coronary artery disease
Dissecting aortic aneurysm (intimal flap, true/false lumen) TOE more sensitive than TTE
PE (dilated right heart chambers ± clot in pulmonary artery) Moderate to large embolus
Pericarditis Effusion often too small to diagnose with echocardiography
Aortic stenosis Clinical signs of stenosis may be absent

AR, aortic regurgitation; ARDS, acute respiratory distress syndrome; AS, aortic stenosis; ASD, atrial septal defect; IABP, intra-aortic balloon pump; IPPV, intermittent positive-pressure ventilation; LA, left atrium; LAA, left atrial appendage; LV, left ventricle; LVOT, left ventricular outflow tract; MR, mitral regurgitation; MS, mitral stenosis; PE, pulmonary embolism. PEEP, positive end-expiratory pressure; RA, right atrium; RV, right ventricle; RVH, right ventricular haemorrhage; RWMA, regional wall motion abnormality; SAM, systolic anterior motion; TOE, transoesophageal echocardiography; TR, tricuspid regurgitation; VSD, ventricular septal defect.

As a general rule, unless there is gross haemodynamic instability or some other overriding reason, the echocardiographic examination should be structured around a basic set of 2-D views. This applies to both TTE and TOE. The focus of the TOE examination should be on the most important specific clinical question. The second priority should be other potential pathology in the differential diagnosis. A printed report should be performed after each echocardiographic examination and should be stored and available for future reference.13

VALVULAR HEART DISEASE14,15

Echocardiography is the ‘gold standard’ for evaluating valvular heart disease. 2-D echocardiography provides excellent imaging of all cardiac valves. Various Doppler techniques allow accurate haemodynamic evaluation of the valves.

VALVULAR STENOSIS

Narrowing or stenosis of any heart valve obstructs blood flow, increasing velocity and causing a pressure gradient across the valve. Evaluation of valvular stenosis requires: (1) imaging of the valve to define the morphology and mobility of the valve cusps; (2) some quantification of the degree of stenosis; and (3) the effect of pressure overload on relevant cardiac chambers. Transvalvular pressure gradients (ΔP) can be estimated by Doppler techniques (see above). Note that in conditions of low cardiac output, pressure gradients will be low, thereby underestimating the severity of stenosis.