Adverse events during diagnostic right and left heart catheterization are more likely to occur in high-risk patients (Table 8-1). Procedural indications should be reviewed carefully to justify the increased risk. An adverse outcome can be avoided by identifying a high-risk patient, implementing preventive measures, and recognizing complications early.
General preventive measures include correction of any electrolyte abnormalities prior to the procedure; awareness of any pre-existing atrioventricular (AV) nodal block, bundle branch block; or prolongation of the QT on the baseline surface electrocardiogram (EKG) to identify patients at risk for procedural arrhythmias. For patients with renal insufficiency, the amount of contrast dye should be minimized and bi-plane imaging considered when available.
Table 8-1 High-Risk Patients
Left main coronary artery disease
Severe ventricular dysfunction
Severe aortic valvular stenosis
Aortic dissection, aneurysm, or atheroma
Cardiogenic shock
Acute coronary syndrome
Hypertrophic obstructive cardiomyopathy
Coagulopathy or increased bleeding risk
Severe pulmonary hypertension
Acute/chronic kidney disease
Peripheral vascular disease
Common Problems in High-Risk Patients
Hypotension:
Periprocedureal hypotension may be caused by contrast allergy or contrast-induced vasodilation, vagal response, ischemia, dysrhythmia, hypovolemia, oversedation. It is important to follow a simple algorithm to identify and treat the cause. First, ascertain that hypotension is real and not caused by artifact (i.e., catheter damping or whip). At the same time, identify any changes in rhythm or ST segments. Next concentrate on complications related to the last task performed (Table 8-2). For example, hypotension or dampening of the pressure waveform during attempts to engage the diagnostic catheter into the left main (LM) or right coronary artery should immediately raise concern for severe ostial disease, iatrogenic vasospasm, or coronary dissection. This is especially true when engaging coronary arteries with anomalous origin or in patients with heavily calcified and diseased aortas in which a greater degree of catheter manipulation or torque was required.
Table 8-2 Troubleshooting Acute Hypotension in the Lab
Severe ostial disease Vasospasm Iatrogenic dissection
Catheter withdrawal Nitroglycerin 50-200 μg IC PCI or bypass surgery
RCA contrast injection
Vagal stimulation Myocardial ischemia
Avoid over-injection of dye Coronary revascularization
Vascular access (immediate)
Vagal stimulation
Self-limited Atropine 0.5-1 mg IV
Vascular access (delayed)
Bleeding
Volume resuscitation Transfusion Vascular surgery evaluation
Crossing the aortic valve
Aortic dissection Coronary dissection
Emergent surgical correction PCI or bypass surgery
PA catheter or wire manipulation in the RV
RV perforation Cardiac tamponade
Volume resuscitation Pericardiocentesis with drain
PA catheter balloon inflation
Arterial rupture
Volume resuscitation Emergent surgical correction
Transvenous pacing wire
RV perforation
Pericardiocentesis with drain
Immediately post-shock for tachyarrhythmia
Electromechanical dissociation
Fluoroscopy to verify cardiac loss of cardiac motion ACLS protocol for PEA arrest
Hypotension during vascular access is typically vagal-mediated, self-limited and it occurs within minutes of vascular manipulation. Hypotension 30 minutes to 12 hours after vascular access should raise suspicion for retroperitoneal bleeding. Patients commonly complain of unilateral flank or back pain. Hypotension immediately following contrast dye injection of the right coronary artery can also be vagal mediated. Having a patient cough may help clear contrast from the coronary circulation and restore normal heart rate. Typically, the right coronary artery is more likely to spasm when engaged compared to the LM trunk. Both effects are heightened by the presence of flow-limiting coronary lesions, and mitigated by precise catheter control and a smooth engagement technique without allowing the tip of the catheter to become deeply seated.
Hypotension during diagnostic right heart catheterization may be attributable to multiple causes. Forceful advancement of the pulmonary artery (PA) catheter within the right ventricle with the balloon deflated or with the tip deflected away from the outflow tract can result in free wall perforation and tamponade. Similarly, the use of a 0.25-in guidewire when attempting to direct the PA catheter beyond the outflow tract in a dilated and/or dysfunctional ventricle can also easily perforate the right ventricular free wall. An abrupt increase in ventricular ectopy with hypotension while manipulating the catheter or wire in the right ventricle should immediately alert the operator to this possibility. Aggressive volume expansion is usually the only measure needed to support patients with iatrogenic right ventricular perforation. Pericardiocentesis with a drain may be necessary in selected cases.
Bradycardia:
Transient bradycardia caused by ionic contrast agents or hypervagotonia usually resolves without treatment. If bradycardia does not resolve spontaneously, treatment with atropine 0.5 to 1 mg IV or more rarely a continuous infusion of dopamine may be required. A temporary transvenous pacemaker (TVP) may be required in selected cases. A typical presentation requiring temporary pacing support involves a patient with a pre-existing left bundle branch block who develops complete or high-grade AV block while manipulating a catheter in the right ventricle during a right heart catheterization. Prophylactic TVP placement should be considered in these patients. A prophylactic TVP is not indicated for first-degree AV block or Mobitz I second-degree heart block.
General indications for TVP also include symptomatic or hemody-namically significant bradycardia attributable to sinus node dysfunction, high-grade atrioventricular block, and enhanced vagal tone (Table 8-3). Blunt-tipped passive placement (i.e., “contact”) pacing wires are most commonly selected as they are easy to use, readily available, and generally atraumatic. It is important to remember to select the pacemaker wire with the preformed curvature appropriate for the vascular access site. Passive temporary wires designed for jugular and subclavian access have a smooth terminal curvature (similar to a PA catheter) to allow the wire to be advanced into the right ventricular outflow tract (RVOT) and pulmonary artery and then gently withdrawn into the right ventricle (RV) where counterclock torque will nestle the tip up along the RV floor at or near the apex. Advancing the wire up into the RVOT and the PA outside of the cardiac silhouette is important to ensure the wire has not inadvertently passed into the coronary sinus (CS). These wires are not designed for CS pacing. Passive blunt-tipped pacing wires designed for femoral access typically have a J-tipped curvature. Under fluoroscopy, the wire is advanced up into the inferior vena cava (IVC) across the tricuspid valve where the curved tip is directed posteriorly and inferiorly along the RV floor at or near the apex. In patients with right ventricular enlargement, straight or curved balloon-tipped temporary wires are also available.
Table 8-3 ACC/AHA Indications for Transvenous Pacemakers in the Setting of Myocardial Infarction
Class I
Symptomatic bradycardia
Bilateral bundle branch block
New or age indeterminate bifascicular block with PR segment prolongation
Mobitz type II second-degree AV block
Class IIa
New or age indeterminate right bundle branch block (RBBB) with left anterior fascicular block (LAFB) or left posterior fascicular block (LPFB)
RBBB with prolonged AV conduction
New or age indeterminate left bundle branch block (LBBB)
Incessant ventricular tachycardia for overdrive pacing
Recurrent sinus pauses greater than 3 seconds not responsive to atropine
Class IIb
Bifascicular block of indeterminate age
New or age indeterminate isolated RBBB
Class III
Prolonged AV conduction
Mobitz type I second-degree AV block with normal hemodynamics
Accelerated idioventricular rhythm
BBB or fascicular block known to exist before myocardial infarction
Adapted from Antman EM, et.al. ACC/AHA Guidelines for the management of patients with ST-Elevation myocardial infarction—Executive summary. Circulation 2004;110:588-636.
Active fixation temporary wires are also available and are typically advanced into the appropriate chamber under the guidance of a 6 or 7 Fr. size stiff outer sheath. The outer sheath is directed to the desired location under fluoroscopy approximately 0.5 to 1 cm away from the wall. The wire is then advanced beyond the sheath to the wall and torqued clockwise to screw it into place. Gently retracting the outer sheath and testing capture thresholds verifies appropriate fixation. Active fixation wires are particularly helpful for atrial pacing, when getting a stable position with good capture is often difficult with the blunt-tipped passive wires. The outer sheath must be carefully advanced and never allowed to tent the myocardium.
Regardless of wire selection, pacing output should be initiated under fluoroscopy. Sudden diaphragmatic movements tracking pacemaker spikes indicate diaphragmatic pacing requiring lead repositioning. The capture threshold, defined as the lowest current necessary for capture, should be established. Output is generally started at 5 mA and slowly decreased until capture is lost. Once the capture threshold is obtained (ideally less than 1 mA), the output is set to two to three times the capture threshold as a safety margin. Sensing thresholds are then tested by setting the pacing rate 10 to 20 beats below the intrinsic rate with the pacemaker in its most sensitive setting (lowest mV recognition available). The sensitivity is then gradually increased until asynchronous pacing occurs. This is the point at which the device can no longer detect the native QRS complex because the threshold has been set higher than the amplitude of the native complex. The pacemaker is then programmed to sense at 50% of the sensing threshold as a safety margin.
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