TSRA Content:
Author: Najah Adreak, MD, MSc
This is a revision and update from the previous edition of the TSRA Primer in Cardiothoracic Surgery written by Najah Adreak, MD, MSc.
Post MI Ventricular Septal Defect (VSD)
When a coronary ischemic event leads to extensive myocardial damage, the ventricular wall is at risk for rupture. The most commonly involved section of the myocardium is the septum due to occlusion of either the left main or left anterior descending artery.
Typically, a post-MI VSD presents within the first week after the MI with a sudden change in clinical status - usually with some degree of cardiogenic shock and a new holosystolic murmur. While there are many etiologies for a post-MI patient to decompensate, early recognition of a VSD is imperative as it is a true surgical emergency.
Recognizing the "sick" patient is the first step. If you suspect a VSD based on history and exam, alert your senior/fellow/attending while you continue your work up and treatment.
The patient should be stabilized in the standard fashion: airway control (e.g. does the patient need to be intubated?), breathing, and circulation (central line, arterial line). Any patient with suspected VSD needs to be transferred to the CTICU for close monitoring and possible inotropic, vasopressor or mechanical support.
To ensure cardiac output, your goals are to give sufficient intravascular volume, increase inotropy and reduce afterload. An intra-aortic aortic balloon pump (IABP) can decrease afterload and maximize coronary perfusion.
Confirming the diagnosis often includes imaging of the heart via echocardiogram. A transthoracic echocardiogram will reveal left to right shunt and other potential causes of decompensation. A Swan-Ganz catheter will demonstrate increased oxygenation in the pulmonary artery indicating a left to right shunt. Catheterization can evaluate coronary disease and a ventriculogram can characterize the size of the shunt, which is enormously helpful in identifying the defect.
If the patient has a VSD, immediate surgery should be tailored to the patient's underlying cause of ischemia. CABG is performed for the diseased arteries. Around the septal defect, a circumferential pericardial (or Teflon felt) patch is sewn to the healthy myocardium overlapping the areas of the defect/necrosis to eliminate the shunt.
Ventricular Rupture
Ventricular (free wall) rupture presents similarly to VSD, except there is no PA oxygen step up on the Swan catheter. (This means the venous and arterial oxygenation levels remain discrete with no mixing between the right and left heart). Echocardiography may show a thin ventricular wall with signs of aneurysmal disease, intra-myocardial hematoma or pericardial fluid. In the latter case, fluid should not be tapped for fear of unroofing a complete rupture causing immediate exsanguination even if there are signs of tamponade. Instead, plans should be made for controlled exploration in the operating room. Repairs generally have good outcomes if the area of infarcted tissue is discrete. .
Cardiac Tamponade
In the post-operative period, you will need to evaluate patients for tamponade physiology and determine the need for re-exploration. This clinical scenario ranges from insidious to a life-threatening emergency. After cardiac surgery, tamponade is most commonly due to mediastinal bleeding. Therefore achieving excellent hemostasis prior to sternal closure is the best prevention. Once the chest is closed in the OR, chest tube outputs should be monitored closely for signs of ongoing bleeding that would prevent the patient from being transported. (This also depends on the patient, procedure, and any known coagulopathies.) Every cardiac center or surgeon will have their own threshold for re-exploration, but as a general guide, the following outputs warrant a re-exploration:
* > 700-1L in first hour
* > 400 ml/h for 2 hours
* > 300 ml/h for 3-4 hours
* > 200 ml/h for 4-5 hours
Keep in mind that sudden cessation of chest tube output may be due to obstruction by clot. Recognizing tamponade physiology is an essential and fundamental skill of the cardiothoracic surgery house staff.
Tamponade arises when fluid accumulates around the heart. The external compression causes an equilibration of pressures on the heart’s four chambers leading to elevated filling pressures, decreased cardiac output and hypotension.
On physical exam, Beck's triad (distended jugular vein, low blood pressure, and muffled heart sounds) may be present, but also may be absent despite a correct diagnosis. On occasion, cardiac output may vary with respiration as intrathoracic pressure influences preload and afterload. As the extrinsic pressure increases, patients often require increased inotropic and/or vasopressor support. As there is a drop in cardiac index, the urine output decreases. The lactate will also rise due to decreased tissue perfusion.
A CXR is a good, but insensitive, initial test revealing an enlarged heart or a widened mediastinum suggesting fluid accumulation. The classic ECG finding is decreased voltage, but there may be any number of non-specific abnormalities. An echocardiogram should be done expeditiously if the patient is not in extremis. A bedside transthoracic (TTE) echocardiogram is usually adequate to make the diagnosis, but a trans-esophageal echocardiogram (TEE) may be necessary if the anterior heart cannot be visualized. A large pericardial collection and RV collapse in diastole are fairly specific signs.
When faced with a hemodynamically unstable patient in the postoperative period, ALWAYS have cardiac tamponade high on your differential.
Re-Exploration
Re-exploration is preferably performed in the operating room, but imminent arrest may require emergency bedside re-sternotomy. If you are forced to open the chest at the bedside, the following must be readily accessible in your ICU or step-down units:
* Betadine prep
* Mask, gown, gloves
* Scalpel (10 or 20 blades)
* Open thoracotomy tray:
- wire cutters
- heavy needle holder
- sternal retractor
* Suction/ irrigation
-Sterile sponges/towels
While you prepare to open the chest, ACLS protocols should be followed in the case of arrest, including attention to the airway, breathing and circulation.
To open the chest emergently, incise the midline with a knife or scissors (if recent operation). A second parallel incision can be made in the presence of staples. Remove sternal wires using a combination of wire cutters and a heavy needle holder. Remember that freshly fashioned bypass grafts may be just below the sternum. Once the chest is open, insert the sternal retractor and visualize the heart. In the case of arrest, begin manual cardiac massage by squeezing from the apex towards the base to promote ventricular ejection out to the aorta. Evacuate blood and clot in the mediastinum. If the cause for the bleeding is readily identifiable, place one finger over the site and look for other sources, taking care not to injure grafts or previous operative sites. Suction and irrigate (+/- antibiotic solution). Remember: your goals are to alleviate the effects of tamponade and decrease life-threatening bleeding until a more experienced surgeon arrives or plans are made for definitive care in the OR.
Prosthetic valve thrombosis (PVT):
Prosthetic valve thrombosis is a severe but rare complication of valve replacement; the mortality rate associated with PVT is approximately 10%, independent of treatment modality. Thus, a high level of suspicion is warranted, and urgent treatment is required. PVT could be obstructive or non-obstructive. The non-obstructive one usually presents with small non- obstructive thrombus or systemic emboli in the early postoperative period, while obstructive PVT presents with valvular obstruction and likely immediate cardiogenic shock. The PVT incidence is higher in mechanical valves compared to bioprosthetic valves. The latter may manifest by incomplete embolization of the suture zone in the early postoperative period.
Pathophysiology:
Hemodynamic, endothelial, and hemostatic factors can lead to thrombus formation on the newly replaced valve. In addition, location of the prosthesis plays an essential role in thrombus formation. Obstruction of tricuspid valve prostheses is 20 times more common than left-sided valves, due to lower pressure; similarly, mitral valve PVT is 2-3 times higher than aortic PVT due to lower pressure across the valve with less turbulence of flow. Optimization of anticoagulation in the early postoperative period is crucial. The balance between over-anticoagulation with risk of bleeding or under-anticoagulation with risk of thrombosis should be carefully considered postoperatively.
Diagnosis of PVT:
The clinical presentation varies depending on the presence or absence of obstruction. Severe obstructive PVT presents with overt heart failure while PVT without obstruction presents with restriction of one valve leaflet and dyspnea, systemic embolism, or fever. The non-obstructive PVT may be found accidentally or present with embolic episodes.
On physical examination, you may find muffling or absence of prosthetic click or appearance of a new murmur. The initial workup includes a transthoracic echocardiogram and cinefluoroscopy for mechanical valves. TOE could be used too. Echo could show reduced valve mobility, the presence of thrombus, elevation of trans-prosthetic valvular gradients and reduced effective orifice area of the prosthetic valve.
Treatment:
Once the diagnosis of PVT is confirmed, the treatment options include surgery, fibrinolysis, heparinization or optimization of anticoagulation and antiplatelet therapy. Large and obstructive thrombi require aggressive treatment with surgery, while fibrinolysis is reserved for high-risk surgical patients.
References:
1.Roudaut, R., Serri, K., & Lafitte, S. (2007). Thrombosis of prosthetic heart valves: diagnosis and therapeutic considerations. Heart (British Cardiac Society), 93(1), 137–142. https://doi.org/10.1136/hrt.20...
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