SEM 2 Lab 1 - Xrays & ECG Flashcards
Interpret
CXR findings - Leadless pacemaker; right atrial and right ventricular retained cardiac pacemaker tips, from the previous left pectoral dual lead pacemaker; internal fixation of the sternum with wires, plate and screws.
Identify
Wiireless pacemaker device
A Micra device is a small wireless pacemaker device, that is transfemorally implanted in the apex of the right ventricle.
Close up view of the Micra device.
Discuss.
The images show a pacemaker with an atrial and ventricular lead.
The tip of the atrial lead is pointed upward and anteriorly, because the ideal position is in the right atrial appendage, where it is anchored within the coarse trabeculae.
The tip of the ventricular lead is positioned in the apex of the right ventricle, which is located to the left of the spine on a frontal chest X-ray and anteriorly on a lateral view.
Bottom right example of an ICD with wires in the right atrial appendage, the apex of the right ventricle and a lead to the left ventricle in the posterior coronary vein.
You can recognize the two shock coils of the ICD as thicker white bands along the course of the lead.
Interpret
ECG 1: Ventricular pacing at a rate of150-200. It is a pacemaker-induced ventricular tachycardia, due electronic failure. It can also occur in certain circumstances where ventricular extra-systoles occur, such that they don’t inhibit the pacemaker output, resulting in a ventricular tachycardia, or when a ventricular beat is not sensed by the pacemaker and ventricular pacing is delivered resulting in a ventricular tachycardia.
Interpret
ECG 2: Paroxysms of rapid pacing spikes at 2000 bpm with decreasing amplitude and rate — this fails to excite the ventricles due to the low amplitude spikes. The underlying rhythm is atrial flutter with 3rd degree AV block and ventricular escape rhythm at 30 bpm. In the middle, three pacing spikes are seen at 60 ppm in VOO mode: the first is ventricular refractory (failed capture).
Interpret
ECG Interpretation:
There is a rapid ventricular-paced rhythm (120 bpm) with no evidence of preceding atrial activity (except for the first complex). The differential diagnosis of this rhythm would include: pacemaker-mediated tachycardia (with retrograde P waves buried in the QRS complexes /T waves), sensor-induced tachycardia, could potentially be normal in the presence of an appropriate physiological stimulus (e.g. exercise, catecholamine ).
Pacemaker-mediated tachycardia is an endless-loop tachycardia, sustained, in part, by the presence of the pacemaker. Pacemaker-mediated tachycardia requires the presence of retrograde ventriculoatrial conduction and a triggering event like premature ventricular contraction or loss of AV synchrony. Pacemaker-mediated tachycardia is similar to a re-entrant tachycardia, except that the pacemaker forms part of the re-entrant circuit; the tachycardia could therefore be avoided by programming a sufficiently long postventricular atrial refractory period (PVARP).Placing a magnet on the device during the PMT will change the pacemaker’s mode to dual-chamber pacing mode (in DOO, intrinsic P waves and R waves are ignored), which results in the termination of tachycardia by suspending the pacemaker’s sensing function
Identify
A dual chamber pacemaker. The atrial lead usually curves upward in a “J “ to reach the atrial appendage. The right ventricular lead (ideally) ends in the ventricular apex to the left of the spine
Interpret
Presence of pacemaker spikes without appropriate capture (green arrows) and a ventricular escape rhythm which can be identified by an absence of P waves prior to the QRS complex (purple arrows).
Identify
CXR interpretation - Cardiac resynchronisation device in the soft tissues of the anterior wall of the chest, contacting the left pectoral muscle. The three electrodes of the cardiac device are retracted, without contact with the myocardium, and whose distal ends are located in the superior vena cava, confluent subclavian-jugular and left subclavian. The cardiac silhouette is enlarged. Pulmonary edema in the interstitial phase.
Interpret
ECG 1: This ECG shows a ventricular paced rhythm with intermittentfailure to capture: Atrial sensing appears to be intact — ventricular pacing spikes follow each P wave, most easily seen in V3-6 (tiny pacing spikes are also visible in I, aVR and V1). There is presumably an underlyingcomplete heart blockorhigh-grade 2nd degree AV block, as the native P waves do not capture the ventricles.
How do you approach a pacer patient? Hint. Pneumonic
75-year-old male patient with a history of ischemic cardiomyopathy and AICD placement presented to hospital after a fall at home and syncopal episode. Vital signs: GCS 15, RR 20, HR 75, BP 94/60(71), SpO2 96%.
As you are doing your physical assessment, he suddenly complains of dizziness with palpitations. ECG 1 is obtained.
Interpret
ECG - Patient converted to monomorphic ventricular tachycardia (VT).
While you are reading ECG1, ECG 2 is obtained, and the patient becomes obtunded. The patient then cries out in pain and ECG 3 is obtained.
ECG 2: Patient in monomorphic ventricular tachycardia (VT) initially. The 8 pacer artifacts indicateanti-tachycardia pacing(burst pacing). However, no termination was noted. Instead, it degenerated to ventricular flutter/ventricular fibrillation (VF).
ECG 3: AICD fired terminating the tachyarrhythmia.
Interpret
Dual lead ICD projects over the left chest
Interpret
ECG 1 – Failure to pace. Deceased or absent pacemaker spikes.
Causes - Oversensing (most common), lead fracture, or insulation defect.
Interpret
ECG 2 – Failure to sense. Pacing spikes within QRS complexes.
Causes – lead insulation break, new intrinsic bundle branch block, electrolyte abnormalities, and class IC antiarrhythmics
List steps to resolve a TVP that is failing to sense.
Inability to detect a depolarization event. Due to specific setting of sensitivity. Decrease absolute value of sensitivity (making it easier to inhibit)https://litfl.com/pacemaker-essentials-undersensing/
Interpret
ECG 3 Failure to capture. Absence of depolarization after pacing spikes.
Functional etiologies include electrode displacement and wire fracture. Pathologic etiologies include ischemia/ infarct and electrolyte abnormalities (especially hyperkalemia)
List steps to resolve a TVP that is failing to capture.
Visible pacing spikes are seen on ECG but no electrical capture on ECG or cardiac contraction seen in arterial line or SpO2 waveform. Usually due to some specific mechanical problem (wires no longer connected to heart, wires not tightly connected to cable, cable not connected to correct port, output setting to low)Other causes: fibrosis at wire-myocardium interface, MI, electrolyte imbalance, post-defibrillation, drugs (flecanide, sotalol, betablockers, lignocaine, verapamil)Approach:⇒ correct exacerbating causes⇒ tight and confirm all external connections⇒ increase output if possible⇒ bipolar leads may be tried in reverse positions or can try convert to unipolar pacing⇒ in bipolar leads, the negative electrodes develop fibrosis first -> use other electrode and plug into negative terminal and insert return electrode in the subcutaneous tissue (create unipolar circuit)
Interpret
dual chamber pacemaker. The atrial lead usually curves upward in a “J “ to reach the atrial appendage. The right ventricular lead (ideally) ends in the ventricular apex to the left of the spine
Interpret
Normal CXR. ECG sinus tachycardia
Interpret
Sinus Tachycardia
Interpret
CT abdo - A large hematoma with a fluid-fluid level and another smaller similar one are visible in the right anterolateral abdominal wall. At least four foci of active bleeding are visible within the larger hematoma, which increases in size on delayed images.
Interpret
ECG - Sinus tachycardia, heart rate 125, Q-waves in the first four precordial leads (V1-V4), and an electric alternans with borderline low-voltage pattern.
Interpret
CXR - Large right pneumothorax with evidence of tension - mediastinal shift to the left and slight hyperexpansion of the right hemithorax.
GCS 13, RR 28, HR 138, BP 82/38, SpO2 89% NRB, Temp 39.6.
Interpret
CXR interpretation – Right upper lobe patchy consolidation, with no cavitation, associated with prominent perihilar and infrahilar markings. There was no pleural effusion or pneumothorax
Interpret
Sinus Tachycardia
Internet
Normal Findings
On assessment - GCS 13, RR 16, HR 28, BP 86/50(62), SpO2 94%, Pupils 4+, Temp 35.8.
Interpret
ECG interpretation – Sick sinus syndrome: sinus bradycardia.Rate down to 12 bpm at times.No complexes recorded in leads V1–V3.
On physical exam, the patient is cool, pale, and edematous with moderate mottling in his extremities. GCS 15, RR 36, HR 128, BP 88/65, SpO2 92%, Temp 36.4.
Labs: WBC 18.8, TnI 143 ng/L. pH 7.21(v), pCO2 34, HCO3 17.
Interpret
CXR -dilated cardiomyopathy. Globular enlargement of the cardiac shadow
Interpret
ECG – Evidence of myocarditis. Sinus tachcardia with widespread STE without reciprocal changes. Low voltage.
