18.1 ICDs, Pacemakers, Occluders, Closure Devices, and Mechanical Support

Recognize the route before naming the hardware

CCI task D12 is to recognize implanted devices such as ICDs, pacemakers, LAA occluders, closure devices, and mechanical support. Start with the access route and endpoints. A transvenous RA lead often curves into the appendage; an RV lead crosses the tricuspid valve toward the apex or septum. A CRT coronary-sinus lead courses posteriorly in a coronary vein rather than entering the LV cavity. An ICD lead usually has one or more thick echogenic shock coils. Subcutaneous or leadless systems have different appearances, and echo cannot reliably identify manufacturer, programming, battery status, or electrical performance. Reconcile the image with device records, interrogation, and chest radiography.

Use electrophysiology to interpret timing and devices

Electrical activation precedes and organizes mechanical motion. The sinoatrial node initiates atrial depolarization, represented broadly by the P wave. Conduction slows through the AV node, allowing ventricular filling, then travels through the His bundle, right and left bundle branches, and Purkinje network to produce a coordinated QRS and ventricular contraction. ECG timing is a reference, not a substitute for visible valve events: conduction delay, pacing, preexcitation, and electromechanical delay can shift aortic or mitral closure relative to automated markers.

Rhythm changes both acquisition and physiology. Atrial fibrillation removes consistent organized atrial contraction and creates variable R-R intervals, so Doppler and chamber measurements require representative cycles rather than the first convenient beat. Atrial flutter may have regular atrial activity with fixed or variable AV conduction. AV block can dissociate atrial and ventricular timing. Premature beats change filling, contractility, and the following postectopic beat; neither beat should be used as an ordinary baseline measurement. Bundle-branch delay and ventricular ectopy can create abnormal septal timing that resembles regional dysfunction if ECG and multi-view motion are ignored.

RV myocardial or apical pacing activates the ventricles outside the normal His-Purkinje sequence and may produce a left-bundle-branch-like pattern, early septal motion, delayed lateral contraction, and mechanical dyssynchrony. CRT adds an LV lead, usually through the coronary sinus, to improve activation coordination in selected patients, but echo appearance alone cannot prove electrical capture, sensing, battery state, or optimal programming. Correlate ECG morphology and rhythm with interrogation. During echo, document the paced or intrinsic rhythm, choose comparable beats, interpret septal motion in that context, and reserve programming changes for the electrophysiology/device team.

Examine leads and closure devices systematically

Follow every visible lead in two planes. At the tricuspid valve, look for leaflet impingement, adherence, entanglement, perforation, restricted coaptation, and the origin and severity of TR. Compare RV and RA size/function and estimate pressure when valid. A mobile lead-associated echodensity may represent fibrin, thrombus, vegetation, redundant lead, or artifact. Describe size, attachment, mobility, and image quality; fever, cultures, pocket findings, embolic events, TEE, and sometimes CT or metabolic imaging establish the clinical diagnosis. Do not call endocarditis from an incidental strand or exclude it because TTE is negative.

A lead tip apparently beyond myocardium should be confirmed in orthogonal views with altered gain and depth. New chest pain, capture failure, hypotension, or pericardial fluid makes perforation more concerning. Immediately communicate a convincing extracardiac course, enlarging effusion, chamber collapse, or deterioration. Echo shows the anatomic and hemodynamic findings; electrophysiology and clinical teams integrate interrogation and cross-sectional imaging and decide management.

An ASD/PFO occluder commonly appears as two discs straddling the atrial septum. Show that both discs are apposed, septal tissue lies between them, and the device does not distort the aortic root, pulmonary veins, coronary sinus, or AV valves. Sweep low-Nyquist color across the full circumference for residual shunt and state its location and direction. A small early residual jet may evolve, so compare with timing and prior studies. Device instability, embolization, new obstruction, pericardial effusion, or suspected erosion is urgent. Failure to see a complication on limited TTE does not replace TEE, ICE, CT, or fluoroscopy when concern persists.

LAA occluders are often incompletely assessed by TTE. TEE or CT more reliably shows device compression, depth, peri-device flow, device-related thrombus, and adjacent pulmonary-vein or mitral interaction. Describe an echogenic surface mass as suspected material until artifact and normal device components are excluded. Other closure devices at a VSD, PDA, paravalvular leak, or access site must be localized to the treated defect; use color to test residual flow and CW only after the jet's origin is established.

Map mechanical support and its hemodynamic effect

A durable continuous-flow LVAD usually drains through an LV apical inflow cannula directed toward mitral inflow and returns blood through an outflow graft to the ascending aorta. Record device type, speed, estimated flow and power shown on the controller, blood pressure, rhythm, and symptoms. Assess LV size and unloading, septal position, RV size/function, IVC, MR/TR, aortic-valve opening frequency, AR, thrombus-like material, and pericardial fluid. Use color and spectral Doppler along inflow and accessible outflow segments, comparing velocity and waveform with device-specific expectations and the patient's baseline. One high velocity does not prove obstruction if angle, aliasing, graft curvature, speed, and loading are unknown.

A very small LV with leftward septal shift, intermittent inflow disturbance, or ventricular ectopy can accompany excessive unloading or a suction event; underfilling, RV failure, tamponade, or cannula malposition may contribute. A dilating LV, more frequent aortic-valve opening, worsening MR, abnormal cannula flow, or rising device power may suggest inadequate support or obstruction, but echo alone does not diagnose pump thrombosis. Search for progressive AR, RV failure, inflow/outflow obstruction, infection-related collections, and intracardiac thrombus. Speed changes belong to the authorized LVAD team during a standardized ramp protocol.

Temporary devices are recognized by route. An axial-flow transaortic pump crosses the aortic valve with an LV inlet and an aortic outlet; its depth and orientation are model specific. TandemHeart drains the LA through a transseptal cannula and returns flow arterially. VA-ECMO drains systemic venous blood and returns it to the arterial circulation; assess LV distention, aortic-valve opening, stasis, RV/LV function, cannula position when visible, and pericardial complications. An IABP lies in the descending aorta and inflates in diastole, then deflates before systole. For every device, label what is actually seen, compare with the prescribed configuration, and urgently escalate migration, perforation, tamponade, severe valve injury, absent expected flow, marked chamber distention, or shock.