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Colombian Journal of Anestesiology

Print version ISSN 0120-3347

Rev. colomb. anestesiol. vol.37 no.4 Bogotá Oct./Dec. 2009

 

CASE REPORT

Complete heart blockage in single ventricle patient having undergone a cardiac catheterization

Mauricio Calderón*, Oscar David Aguirre**, Angela María Ríos**, Hernán Darío Jaramillo**

* Médico anestesiólogo, Hospital Santa Sofía. Profesor, Facultad de Ciencias de la Salud, Universidad de Caldas, Manizales. E-mail: caldero2001man@yahoo.es

** Médico general. Residente de Anestesia y Reanimación, Universidad de Caldas, Manizales.

Recibido: Octubre 1/2009 Aceptado: Diciembre 11/2009


Male patient, two years old, programed for a cardiac catheterization as a follow-up to the presentation of single ventricle type of cardiac pathology (SV). Previous cerclage of pulmonary artery of one year as temporary management (after this procedure, pulmonary artery systolic pressure (PASP): 31mmHg).

An active physical examination with no dyspnea or oxygen support revealed the following: peripheral cyanosis and signs of digital clubbing, conservative vesicular murmur, and a grade IV systolic murmur mainly in the mitral valve. Cardiac frequency- 70; oxygen saturation (SO2)- 78%; fractional inspired oxygen (FiO2)- 0.21; blood pressure- 93/40; respiratory frequency- 25; weight- 11 kg; length- 85 cm; distal perfusion- 2 sec.; diminished peripheral pulses. An echocardiogram two months earlier revealed a SV with double entrance and exit, large vessels badly positioned and cerclage of pulmonary artery.

An induction is effected with sevoflurane. The peripheral vein is channeled and the induction is complemented with etomidate- 0.2 mg/kg IV. The endotracheal tube is positioned and the following vital signs are observed: AT- 100/40; CF- 110; SO2- 78%; CO2 espired (ETCO2)- 42; EKG- sinusoidal rhythm in DII. Anesthesia is continued with the sevoflurane. After 30 minutes the hemodynamic procedure is initiated with the following vital signs: AT- 88/36; CF- 98; SO2- 93%; End tidal CO2 , ETCO2- 35mmHg; EKG- sinusoidal rhythm.

Various incidents of temporary desaturation occur. After positioning the first catheter and introducing it at the ventricular level, a ventricular tachycardia is suddenly caused followed by a complete persistent auriculoventricular blockage (see Figure 1) without the occurrence of cardiopulmonary arrest.

Treatment with successive doses of atropine (0.01 mg/kg) is begun and hydrocortisone (5 mg/ kg) is given. A CF of 40 beats and an AT of 60/20 is observed. The patient is stabilized by the placement of a transvenous pacemaker. Patient is taken to ICU in which he remains in stable condition. During the ICU stay he does not require inotropic support; furthermore, his kidney signs, central nervous and cardiovascular systems do not experience complications.

Discussion

Congenital cardiopathies cover a spectrum of pathologies which need multidisciplinary treatments and follow-up. The follow-up is carried out by virtue of susceptibility to pharmacological or surgical treatments, age of patient, pathophysiological conditions and clinical repercussions (1).

Concerning congenital cardiopathies, the SV is considered to be a complex pathology, with an incidence rate of 5/100,000 in newborns and is equally distributed between the sexes (2).

The SV implies an absence of the interventricular septum or presence of a unique ventricular cavity for the systemic and pulmonary flows; nonetheless, due to the physiological impact in the behavior of some pathologies with exit flow obstructions and the susceptibility of these obstructions to a certain type of management similar to that established for the SV, the definition for conditions that the “SV physiology” causes has been broadened. These conditions are those that cannot be repaired by adhering to the concept of biventricular correction (3).

It is imperative that the anesthesiologist know the pathophysiology of congenital cardiopathies and the modifications that arise as the patient grows or as the patient undergoes surgical or medical treatments (4).

The basic concept for the SV is the exit ventricular flow. The volume ejected per time unit into the systemic and pulmonary circulation is determinant in the conservation of gaseous exchange, tissue perfusion, and hemodynamic stability owing to the mixture of the volume of blood, pressure and vascular resistences (5).

Concerning blood flow it is possible for the pulmonary flow (Qp) to be equal to the systemic flow (Qs), a situation which places the pulmonary vascular bed at risk of being harmed and susceptible to pulmonary hypertension (6). If the flow is mainly pulmonary, the irrigation of tissue can be compromised; if the flow is predominantly systemic, it is partially appropriate to a certain point since a Qp/Qs relation less than 0.5 will cause interference in the pulmonary blood oxygenation (7).

In any of the above possibilities the ventricle is burdened with two charges: Qp-Qs, and the work load is greater, thus causing the metabolic consumption and coronary flow to become risk factors for possible miocardic tissue damage.

The completion of procedures such as the cardiac catheterization and echocardiogram allows the determination of anatomical and physiological variables that act as criteria in the process of surgical treatment (8). To carry out a catheterization in a pediatric patient it is customary to choose general anesthesia due to the risk of endovascular trauma when using other techniques; nonetheless, one can equally opt for less invasive strategies (9).

The medication that is recommended includes the following: ketamina, propofol, midazolam and remifentanil in continuous infusions. The inhalation agents are rarely utilized, although on occasions sevoflurane is used. Using local anesthesia at the vascular puncture site is recommended (2).

Goals concerning trans-surgical management should be established inasmuch as the parameters vary completely compared with those of biventricular physiology (10). The management of the O2 and CO2 pressures is important; an increase in the first or a decrease of the second may lead to a diversión of flow toward the pulmonary circulation with a subsequent tissue hypoperfusion. For some authors, after completing the pulmonary protection with cerclage, for example, the effects of manipulating blood gas pressures are lost (11); notwithstanding, it is very important to maintain them as close as possible to the baseline and generate the least change possible in the usual parameters.

Concerning the cardiac catheterization, the worldwide percentage of complications is 8.8% (4); the most common are vascular and cardiac arrhythmias. The latter occur more frequently upon manipulating the catheters and tend to be temporary. The order of arrithmia occurrences is as follows: ventricular extrasystoles, ventricular tachycardia, bradycardias, and complete auriculoventricular blockage.

Concerning cardiac catheterizations, complex cardiopathies such as the SV are considered risk factors for the onset of complications associated with the procedure. This occurrence increases when the cardiopathies have been previously intervened (12).

In the case that is being presented, one sees features highlighted in the literature such as the complexity in the management of patients with congenital cardiopathies, in which, of course, it is important to know the pathophysiological mechanisms and the management that these require, as well as especially trying to maintain the patient in conditions as close to the baseline as possible. This endeavor is not usually considered in classical physiology.

The literature reports a complete auriculoventricular blockage as an expected complication in cardiac catheterization, susceptible to fast management. A notable aspect in this case is the use of steroids in order to manage blockages.

There are few studies related to this topic. The ones that exist focus, in general, on explaining the mechanisms of the steroids, more specifically hydrocortisone, as a hormone that improves the response of the sympathetic nervous system upon inducing intracellular protein syntheses that participate by regulating the permeability of ions. This would have some effect on the response to catecholamines (13,14), but conclusive studies concerning this do not exist.

Conclusions

Upon supplying anesthesia for a patient with congenital cardiopathy, one should establish management goals in accordance with the physiology of the pathology and the baseline conditions of the patient.

The perioperative management in procedures such as the cardiac catheterization of patients with complex congenital cardiopathies should be determined beforehand while considering the possible necessity of ICU management, blood reservation or the availability of electric or endovascular therapy devices by virtue of the high frequency of complications associated with these procedures.

The notification of incidents in the development of diagnostic and therapeutic interventions of patients with congenital cardiopathies allows characterizing them better and optimizing their management.

The effect of steriods in the management of alterations in cardiac electrical conduction has not demonstrated any benefit in a systematic way; nevertheless, in some places the use of these continues. More studies are needed to determine their usefulness.

Referencias

1. Andropoulos DB, Stayer SA, Russell IA. Anesthesia for congenital heart disease. London: Blackwell Pub; 2005.

1. Muñoz R, Da Cruz E, Palacio G, Maroto C. Cuidados Críticos en Cardiopatias Congênitas o Adquiridas. . Bogotá: Distribuna LTDA; 2008.

2. Atz AM, Feinstein JA, Jonas RA. Preoperative management of pulmonary venus hypertension in hypoplastic left heart syndrome with restrictive atrial septal defect. Am J Cardiol. 1999; 83:1224-8.

3. Rincón I. Manejo anestésico del niño con cardiopatía durante el cateterismo cardiaco. Revista Colombiana de Anestesiología. 1996; 24:359.

4. Wessel DL. Simple gases and complex single ventricles. J Thoracic Cardiovascular Surgery 1996; 112: 665-7.

5. Lake CL, Booker PD. Pediatric cardiac anesthesia. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2005.

6. Schwartz S, Dent L, Musa N, Nelson D. Single Ventricle Physiology. Critical Care Clinics 2003; 19: 393-411.

1. Behrman RE, Kliegman RM, Nelson WE, Jenson HB. Nelson, tratado de pediatría. Madrid: Elsevier España; 2004.

2. Francis DP, Willson K, Thorne SAl. Oxigenation in patients with a functionally univentricular circulation and complete mixing of blood: are saturation an flow interchangeable? Circulation 1999;100:2198 -203.

3. Taeed R, Schwartz SM, Pearl JM. Unrecognized pulmonary venous desaturation early after Norwood palliation confounds Qp/Qs as assessment and compromises oxygen delivery. Circulation 2001; 103: 2699-704.

4. Vitiello R, McCrindle B, Nikanem D. Complications associated with pediatric cardiac catheterization. J Am Coll cardiol, 1998; 32: 1432-40.

5. Charris H. Consideraciones anestésicas después de corrección quirúrgica de cardiopatías congénitas. Revista Colombiana de anestesiología. 1996; 24: 365.

6. Hu ZL, Liu H, Hu Y, Zhang DY, Sun ZQ. Effects of hydrocortisone sodium succinate on sodium current in human and guinea pig cardiac myocytes. Yao Xue Xue Bao. Apr 2004;39(4):250-3.

7. Seleznev IM, Martynov AV, Kolpakova GV, Smirnov VN. Calcium and the permissive effect of glucocorticoids: the role of glucocorticoids in an adrenaline-induced increase in the rate of calcium absorption by the ventricular tissue of the rat heart. Kardiologiia. Mar 1979;19(3):76-80.

1. Andropoulos DB, Stayer SA, Russell IA. Anesthesia for congenital heart disease. London: Blackwell Pub; 2005.        [ Links ]

1. Muñoz R, Da Cruz E, Palacio G, Maroto C. Cuidados Críticos en Cardiopatias Congênitas o Adquiridas. . Bogotá: Distribuna LTDA; 2008.        [ Links ]

2. Atz AM, Feinstein JA, Jonas RA. Preoperative management of pulmonary venus hypertension in hypoplastic left heart syndrome with restrictive atrial septal defect. Am J Cardiol. 1999; 83:1224-8.        [ Links ]

3. Rincón I. Manejo anestésico del niño con cardiopatía durante el cateterismo cardiaco. Revista Colombiana de Anestesiología. 1996; 24:359.        [ Links ]

4. Wessel DL. Simple gases and complex single ventricles. J Thoracic Cardiovascular Surgery 1996; 112: 665-7.        [ Links ]

5. Lake CL, Booker PD. Pediatric cardiac anesthesia. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2005.        [ Links ]

6. Schwartz S, Dent L, Musa N, Nelson D. Single Ventricle Physiology. Critical Care Clinics 2003; 19: 393-411.        [ Links ]

1. Behrman RE, Kliegman RM, Nelson WE, Jenson HB. Nelson, tratado de pediatría. Madrid: Elsevier España; 2004.        [ Links ]

2. Francis DP, Willson K, Thorne SAl. Oxigenation in patients with a functionally univentricular circulation and complete mixing of blood: are saturation an flow interchangeable? Circulation 1999;100:2198 -203.        [ Links ]

3. Taeed R, Schwartz SM, Pearl JM. Unrecognized pulmonary venous desaturation early after Norwood palliation confounds Qp/Qs as assessment and compromises oxygen delivery. Circulation 2001; 103: 2699-704.        [ Links ]

4. Vitiello R, McCrindle B, Nikanem D. Complications associated with pediatric cardiac catheterization. J Am Coll cardiol, 1998; 32: 1432-40.        [ Links ]

5. Charris H. Consideraciones anestésicas después de corrección quirúrgica de cardiopatías congénitas. Revista Colombiana de anestesiología. 1996; 24: 365.        [ Links ]

6. Hu ZL, Liu H, Hu Y, Zhang DY, Sun ZQ. Effects of hydrocortisone sodium succinate on sodium current in human and guinea pig cardiac myocytes. Yao Xue Xue Bao. Apr 2004;39(4):250-3.        [ Links ]

7. Seleznev IM, Martynov AV, Kolpakova GV, Smirnov VN. Calcium and the permissive effect of glucocorticoids: the role of glucocorticoids in an adrenaline-induced increase in the rate of calcium absorption by the ventricular tissue of the rat heart. Kardiologiia. Mar 1979;19(3):76-80.        [ Links ]