Open heart surgery for a left atrial mass extraction during cardio-pulmonary bypass (CPB) in a 9 yoa Labrador dog
Ranko Georgiev1, Stoyan Nikolov2, Nadezhda Petrova3
Georgi Ignatov4, MD Thoracic Surgery
1,2,3 DVM, Central Veterinary Clinic, Sofia, Bulgaria
4 MD, City Clinic Cardiovascular Center, Sofia, Bulgaria
Open heart surgery during a cardiopulmonary bypass is the only effective approach for some diseases that require an access to the heart chambers or the great vessels; even when a temporary inflow occlusion is chosen as an alternative, only a very few “time restricted” procedures could be done on a beating heart. However, when considering an open heart surgery, the high risk of intra- and post- procedure complications often outweighs the benefits. In veterinary medicine the financial weight of such a procedure is also a limiting factor.
We would like to share a case where a temporary sinus arrest was induced during a cardiopulmonary bypass and a huge mass was successfully extracted from the left atrium of a dog with an open heart approach.
Arthur is a 9 year old MC Labrador, trained like a guide dog for a blind person, admitted because of increasingly frequent exercise intolerance episodes during the past few months. Furthermore, the last week the patient was very weak and experienced several syncopal episodes. On a clinical presentation with the referring vet а tachycardia and dyspnea were noted and the patient was referred to us for a Cardiology consult.
On physical examination, the dog weighted 25 kg, with a history of a rapid body mass loss for the last couple of months. His “normal” weight has always been around 32 kg according to the owners. The body condition was poor (score 2/5) and the dog had a grade II/VI left sided apical soft diastolic heart murmur. Lung auscultation was unremarkable, but the respiratory rate (RR) was more than 50 breaths per minute.
The X-rays of the chest were highly suggestive for e left sided congestive heart failure and showed mild generalized cardiomegaly with a VHS of 11.5 with enlarged left atrium and left ventricle. The pulmonary veins were slightly larger than the pulmonary arteries; the lung parenchyma with diffuse interstitial pattern in the area of the hilus. The patient was already on Furosemide in a low dose – 2mg/kg twice a day for the last two weeks with no improvement of the clinical signs.
A transthoracic echocardiography was done with the patient in lateral recumbence through the right and left parasternal windows. A huge echogenic mass with irregular shape was observed in the area of the left atrium – attached to the intra atrial septum and prolapsing through the mitral valve during diastole towards the left ventricle. The mass was creating almost full diastolic obstruction of the valve, allowing only a tiny fraction of the blood in.
Complete blood count, electrolytes and biochemical profile were normal. During the abdominal US study no further abnormalities were noted and no more masses found. On the ambulatory ECG a normal sinus rhythm was recorded with multiple atrial premature complexes. The blood pressure was normal. A hemo-culture and a urine culture were obtained and came back negative for a bacterial growth. The bleeding time and the Pt/APtT were normal.
A diagnosis of an intra atrial mass with clinical signs of a progressing left sided congestive heart failure was made and a surgery was discussed. Because of the location of the mass no surgical or interventional approach was possible without the aid of a cardiopulmonary bypass (CPB) and cardioplegia. All the risks and possible complications were discussed with the owner and a decision for such a surgery was made. The team for the surgery was from a veterinary surgeon, human cardiovascular surgeon, cardiovascular perfusionist, veterinary and human anesthetists, and nurses. The procedure was done in Central Vet Clinic, Sofia on 3rd of December 2016.
Our anesthesia protocol with this patient started routinely for the procedure of a thoracic surgery – premedication with Midazolam and Buprenorphine, induction with Etomidate, intubation and maintenance with Isoflurane. Additionally we put a bladder catheter for urine production measurement, central venous catheter, an intra-arterial catheter for a direct blood pressure measurement and tree peripheral intra-venous catheters. Many more drugs were used during the anesthesia and the long post-operative recovery period like Nitroglycerin, Atracurium, Protamine, Amantadine, Pyracetam, Efedrin, Dopamine, Methylprednisolone, Fraxiparin, Clopidogrel, antibiotics, etc.)
The surgical approach was through the left fifth intercostal space with a standard lateral thoracotomy. Additionally the left carotid artery was approached and prepared in case it is needed for the CPB blood return. The pericardium was excised and the left atrium, the big vessels and the left ventricle visualized. Then three cannulas were put – the one collecting the venous blood inside the right atrium (through the right atrium auricle), the one returning the oxygenated blood from the CPB machine into the ascending aorta and one small cardioplegique cannula into the aortic root over the coronary arteries. Then a bolus of Heparin was injected iv in a dose of 800UI/kg and 5 minutes later the patient was switched to the heart-lung machine (Sorin 5 and a pediatric oxygenator with 360 ml prime). Then we started a controlled cooling of the patient using a chiller, connected to the CPB machine. When the target body temperature of 28o C was reached the ascending aorta was cross clamped and a 600 ml of cooled to 4o C crystalloid cardioplegique infusion rich in potassium was infused through the coronary cannula producing complete heart arrest. We stopped the active ventilation of the lungs and the patient became fully dependent of the heart-lung machine. The heart was open through a 5 cm cut into the left atrial wall starting from the auricle tip. The mass was directly visualized and excised. It was connected to the intra atrial septum with a relatively small neck. We removed it without creating an ASD. The air from the heart was evacuated and the surgical cut closed with a 5-0 Polypropylene suture in a continuous way. The mass was a solid and well defined structure with irregular shape and was admitted for histology. The size was 8/6/4 cm.
We started a slow rewarming of the patient with a target body temperature of 38o C. Two epicardial electrodes were embedded and connected with an external pacemaker. Once closed and warmed, the heart was gently massaged manually for a couple of minutes and then hit with a direct pediatric defibrillator. We used 5 to 20J of energy shocks and got a slow and then faster rhythm after the 9th try. The external pacemaker was switched on and put on a 100 bpm rate for the next 12 hours. The surgical closure was uncomplicated and no significant bleeding was noted. The patient received slowly iv Protamin (1mg/100IU Heparin) as a Heparin antidote and the heart-lung machine was gradually restricted and then switched off. Two chest drains were put and connected to a sterile active suction. The total machine time was 130 min, the sinus arrest time – 22 min, total surgery time – close to 5 hours. Immediately after the CPB machine was stopped a hemotransfusion with two units of fresh blood was done.
Arthur recovered from the general anesthesia slowly over the next 12 hours, but he was unable to stand on his feet for additional 5 days. The electrolyte levels, liver and kidney values were monitored almost every hour for the first 2 days and then three to five times a day; our main concern was the potassium blood level and we tried to maintain it stable at all times. The urine production was also constantly monitored and tailored to be in the normal range – with diuretics and blood pressure control drugs. From all the possible complications after a CPB we saw only a transient neurological signs attributed to some degree of brain injury – interpreted after the neurological exam as left sided forebrain lesion – ischemic or hemorrhagic. Arthur recovered completely both physically and mentally for the next two weeks with a lot of supportive care and physiotherapy. On discharge from the clinic he was able again to do all the things a blind person guide dog is trained to do. The histology report was made in a referral laboratory in Germany – Laboklin, and after the immunohistochemistry stain came back as a Neurofibrosarcoma.
CPB is a routine everyday procedure in the human hospitals, usually carrying a good to excellent prognosis and very low mortality rate. On the other hand in the veterinary medicine field is still an exotic and very risky one. Although very demanding both for the clinical team and the patient himself, the cardiopulmonary bypass is the only option for cardiac diseases requiring an open heart surgery. We believe that a close relationship between a human medicine cardio surgical team and a small animal hospital team could make this type of procedures safer and better recognized.
We have done regular monthly rechecks on the patient with echocardiography and X-rays since then and now six months later Arthur is doing great, no drugs or any supportive therapy needed. He gained back his usual weight and is working like a guide dog every day.
Dr Todor Kalinov
ZaraVet- city of Plovdiv, Bulgaria
Degenerative mitral valve disease (DMVD) is the most common cardiologic disorder in canine population. It has been estimated to account for 75% to 80% of canine cardiac disease1. It is common in small breed dogs, but also can be encountered in large breeds like german shepherd and other . The disease characterizes with thickening and enlarging of the mitral leaflets, elongation of chrdae tendineae and mitral regurgitation. Histopathologic features are expansion of extracellular matrix with glycosaminoglycans and proteoglycans; valvular interstitial cell alteration; and attenuation or loss of the collagen-laden fibrosa layer2. Because of the mitral regurgitation the usual course of this disorder represents volume overloud of the left atrium and left ventricle , eccentric hypertrophy of the left ventricle , dilation of the left atrium ,and left sided congestive heart failure . Increased pressure in left atrium and pulmonary veins leads to pulmonary edema . Often complication is so called passive pulmonary hypertension , consequence of increased pressure in pulmonary veins. Really rare complication is left atrial rupture .
Richka is 12 years old mixed breed dog with history of DMVD , threated only with enalapril . She was admitted in our clinic for cardiologic examination, because recently increasing in coughing and exercise intolerance. During the examination she was tachypneic , normal mucous membrane color , alert and responsive .She had increased heart rate. Auscultation revealed right and left apex systolic heart murmurs. The abdomen was swollen with palpable fluid thrill. We have made echocardiographic examination, with the patient on left and right lateral recumbency, with all parasternal views according to the accepted standards. We found eccentric hypertrophy of the left and right ventricles, left and right atrial dilation, thickening and prolapse of the mitral valve. Doppler examination shows mitral and tricuspid regurgitation with pressure gradient of 162 mmHg and 62 mmHg respectively (figures 1,2,3) . Abdominal echography revealed ascites. So we diagnosed degenerative mitral valve disease with secondary pulmonary hypertension. We prescribed following: pimobendan – 0.25 mg/kg/bid , furozemid – 4.0 mg/kg/bid , spironolactone – 1.0 mg/kg bid enalapril – 0.5 mg/kg/bid , sildenafil – 1.0 mg/kg/tid.
Week later on control examination Richka was better, ascites resolved , mitral and tricuspid regurgitation was with gradient 125 mmHg and 43 mmHg respectively. So we decreased the dose of furosemide to 2.0 mg/kg/bid, and the other drugs were continued with the same doses.
Several months later the owners noticed again swelling of the abdomen and the dog collapsed after exercise. When they came in the clinic Richka was tachypneic with cyanotic mucous membrane. On auscultation we have found 5/6 systolic murmur on the right haemithorax with palpable precordial thrill. Electrocardiography revealed sinus tachycardia – 156 bpm , with premature supraventricular and multifocal ventricular complexes (fig 4). We have made roentgenography in right lateral (fig 5) and dorsoventral (fig 6) position. There was generalized cardiomegaly with dilation of the pulmonary vessels. On echocardiographic examination we have found eccentric hypertrophy of the left and right ventricles, paradoxical motion of the ventricular septum (fig 7), mitral and tricuspid regurgitation with gradient – 118 mmHg and 42 mmHg respectively. Abdominal ultrasonography showed ascites with no collapse of the caudal vena cava with respiration (fig 8). Despite the medications and lower then before pulmonary pressure in this dog the signs of right heart failure were predominant. Because of that and the palpable precordial thrill on the right side we suggested right to left intracardiac shunt. The presence of ventricular septal rupture is less possible, so we decide to search for rupture of the atrial septum. On the right parasternal 4 chambers view modified for better visualization of the right and left atrium with atrial septum, we have found rupture of the septum in the region of the fossa ovalis with left to right shunt.
Video 1 and 2 are same loops with and without colour Doppler demonstrating the defect and shunt of the blood. In this region very often because of the echo dropout on 2d image can be seen a hole in the atrial septum. To be sure that this is a real defect we decided to make a bubble contrast study. We injected 10 ml of agitated saline in v.cephalica antebrachii thru i.v. catheter. When there is right to left shunt the microbubbles are seen in left atrim, left ventricle or arterial circulation – usually the abdominal aorta. But in left to right shunt the goal of the bubble study is to notice contrast washout during right atrium passing of the bubbles. Video 3 and 4 show right parasternal short axis view of the base of the heart with cranial vena cava. We can see the entrance of the contrast and the following washout like a flame because of the left to right shunting of the blood.
In this situation sildenafil makes the pulmonary pressure lower and facilitate the shunt from high pressure left atrium to low pressure right atrium. So we decided to use pulmonary hypertension properly and make the dose of sildenafil lower – 1 mg/kg/24 h. with presumption that higher right ventricle and right atrium pressure will make the amount of the shunt lower. 72 hours after this change the ascites resolves and the condition of the dog became better. On the time of the written of the article Richka is about half year on this medications with sildenafil once per day and no changes in other medications and the only clinical sign is exercise intolerance.
Rupture of the atrial septum is really rare complication of mitral valve disease. Most commonly the rupture occurs in caudal weaker part of atrial wall. In a study of Buchanan JW from 30 dogs only in 4 was found rupture of the interatrial septum with signs of right heart failure3. In another study from the same investigator from 50 dogs 7 have acquired ASD4. The еtiology for rupture of the left atrium is uncleаr , but probably is related with the high pressure in the left and right atrium and the so called jet lesions from the mitral and tricuspid regurgitation. Usually the mitral regurgitation jet is toward lateral wall of the left atrium like in this case (video 5). Tricuspid regurgitation jet was directed to interatrial septum so probably contributed to rupture of the septum. The thin fossa ovalis is weak and suitable place for this kind of lesions. In human medicin rupture of the septum is reported after blunt chest trauma , most often accompanied with rupture of the tricuspid valves 5,6. The proposed reason is that compressivе force occurred during isovolumic contractiоn with maximally dilated ventricles and closed atrioventricular valves5. In humans right ventriсle is right behind the sternum , and this predispоse it to injury. In those cаses when there is rupture of the tricuspid valve and massive regurgitation , the increased pressure in right atrium leads to rupture of the septum and right to left shunt. In canine patients with degenerative mitral valve disease after the rupture of caudal atrial wall and following haemopericardium the clinical signs are collapse and sudden death. After rupture of the atrial septum the predominant signs are of right heart failure. In this case the right atrium and ventricle serves as a low pressure “sink” for severely dilated left atrium.
There are several publications about echocardiographic diagnosis of acquired atrial septal defect and rupture of the atrial septum with haemopericardium3,4. The bubble contrast study has been validated in veterinary echocardiography for diagnosis of congenital and acquired intra and extra cardiac defect and shunt7,8. In this case we have demonstrated the usefulness of so called contras washout – result of bubbles free blood entering contrast rich compartment.
In conclusion in any dog with degenerative mitral valve disease and predominated signs of right heart failure we have to look echocardiographically for atrial septal rupture. More we scan , more we find , and more we learn.
Todor Kalinov, DVM, Zaravet veterinary clinic, city of Plovdiv, Bulgaria, e-mail email@example.com
Patent Ductus Arteriosus(PDA) is one of the most frequently encountered congenital heart disease in dogs , ranging in prevalence from about 25 to 32 % from reported malformations 1 , and lest frequently in cats – about 11 % . The ductus arteriosus is normal foetal structure that shunts blood from pulmonary artery to aorta 2. Before the birth , it divers approximately 80 to 90 % of the right ventricular output back to the left side of the circulation. After parturition and the onset of breathing , pulmonary vascular resistance falls, flow in the ductus reverses , and the resulting rise in arterial oxygen tension inhibits local prostaglandin release causing constriction of the vascular smooth muscle within the vessel wall and functional closure of the ductus arteriosus3.
The ductal wall usually contains a loose branching pattern of circumferential smooth muscle in normal pups. The increasing genetic liability to PDA represents extension of the noncontractile wall structure of the aorta to an increasing segment of the ductus arteriosus, progressively impairing its capacity to undergo physiologic closure1.
In typical cases because of the lower pressure in pulmonary circulation there is continuous flow thru the ductus arteriosus from aorta to pulmonary artery. Clinical impact from this is volume overload of the structures in the shunt pathway : the main pulmonary artery, lungs, left atrium, left ventricle, and back to the ascending aorta up to the level of the ductus4. In that shunt direction the dogs show signs of left-sided congestive heart failure – exercise intolerance, coughing, eventually pulmonary edema. In rare instances when the ductus still wide after birth, the flow is really enormous and this leads to increase in pulmonary vascular resistance and change in direction of the shunt, so-called Eisenmengers physiology and reversed PDA . This pattern of pulmonary hypertension and reversed (right to left) shunting usually develops within the first few weeks of life3. Clinical signs in reversed PDA are shortness of breath, differential cyanosis – pink mucous membranes in cranial part of the body and cyanosis in caudal membranes, polycythemia , pelvic limb weakness, collapse, and seizures. The changes in pulmonary vasculature are irreversible and closure of the PDA is not suggested.
Many dogs with left to right PDA do not show any clinical signs, but if left heart failure has developed in first year of life, up to 65 % would die if left untreated. In most of the dogs clinical signs are apparent before the third year of age. The appearance of signs in older dogs is unusual2.
Buky was 7 years old springer spaniel admitted in our clinic with severe respiratory distress. He had history of heart murmur noted on routine examination , several episodes with increasing respiratory rate, and one presyncopal event with rear limb weakness. All clinical signs were apparent past several months.
The dog breathed with open mouth, mucus membranes were cyanotic , respiration rate increased, and on auscultation we have founded continued heart murmur, and crackles on the both side of the thorax. On the X-ray there was severe generalized cardiomegaly, pulmonary overcirculation with dilation if the pulmonary arteries and veins, interstitial to alveolar lung pattern (Figure 1 – L/L projection, Figure 2 – D/V projection). We have applied initial therapy for congestive heart failure with:
Furozemide – 4mg/kg/hour i.v.
Pimobendan – 0.25mg/kg p.os.
Enalapri – 0.5mg/kg p.os.
Sodium nitroprusside – i.v. constant rate infusion
Oxygen – via mask .
After several hours there was a reduction in respiratory rate, and efforts and an ECG and echocardiography were made.
ECG findings :
Sinus tachycardia – 163 bpm
Wide and tall P wave – suggestive of left atrium enlargement
Tall R wave – suggestive of left ventricular enlargement (Figure 8)
Atrial premature complexes (Figure 3)
Ventricular premature complexes(VPC) with origin in left ventricle (Figure 4)
Fusion beats – intermediate morphology between normal complexes and VPC (Figures 5, 6, 7).
We have made echocardiography at left and right lateral recumbency of the patient with all parasternal views according to accepted standards. From the exam we have found severe left heart volume overloud with eccentric hypertrophy of the left ventricle. Left atrium was dilated with rightward excursion of the atrial septum. Left ventricle was dilated with thin free wall and interventricular septum, dooming of the septum to the right ventricle, and reduced systolic motion of the free wall and the septum (video 1).
Left atrium and aorta was measured on right parasternal short axis view at the heart base and the ratio LA/AO was estimated with results showing at Figure 11. Normal LA/AO ratio have to be < 1,6. Main pulmonary artery was dilated compared to aortic root (video 2)
, and blowing of the pulmonary valve was noted (Figure 12).
On Color Doppler exam there was mild mitral regurgitation with central jet , probably because the dilation of the mitral annulus (Figure 13), and in pulmonary artery was noted typical for PDA continuous flow (video 3).
With CW Doppler the aortic flow velocity was measured 2,19 m/s , with normal speed les then 2.0 m/s. In pulmonary artery CW Doppler show typical continuous bidirectional flow (Figure 14).
On the basis of this findings the dog was diagnosed with Patent Ductus Arteriousus with left to right shunt. Because of the dramatic structural and functional changes in heart, the already developed left heart failure and increased anesthetic risks the owners refused surgical ligation of the ductus. At the time of the diagnosis in our country we did not have the chance for transcatheter coil embolisation. So the only opportunity was to treat congestive heart failure with medications. We have prescribed :
Pimobendan – 0.25 mg/kg/12 h. p.os
Enalapril – 0.5 mg/kg/12 h. p.os
Furozemid – 1.0 mg/kg/12 h. p.os
Spironolacton – 1.0 mg/kg/12 h. p.os
Supplements with L carnitine, taurine, and coenzyme q10.
The dog was very well after the beginning of the therapy and had only exercise intolerance. After about 1 year he had improvement in some echocardiographyc parameters of systolic function – normal fractional shortening, normal pre ejection period, normal ejection time, but the left atrium was bigger then year ago (Figures 15, 16, 17).
Video 4 – right parasternal four and five chamber view year after diagnosis ,
video 5 – modified left parasternal short axis view of heart base with color Doppler of the pulmonary artery showing continuous flow with small turbulent jet in opposite direction.
The treatments for Patent Ductus Arteriosus are surgical ligation or transcatheter device closure. Because of the technical factors and price in our country no one does make device closure but in many clinics surgical procedure can be done with great success. In this case the owners decline surgery, but mine opinion is also that the dog was not appropriate candidate for operation. Despite the fact that in most cases there is dramatic improvement in clinical status and cardiac function after surgical closure, the age ,the already developed heart failure, and concurrent heart disease, affect negatively survival period after PDA closure5. In adult dogs one of the major surgical complications is haemorrhage due to ductus friability2. Mitral valve endocardiosis is also an important factor affecting the survival period. On video 1 and 4 we can see the slight thickening and prolapsed mitral valve leaflets, so I supposed that the dog had degeneration of the mitral valve. Conduction instability of the heart is another reason for anesthetic complications. Actually the dog has died suddenly during routine walk without any other signs, about two years after the diagnosis, so malignant arrhythmia can be the reason. Despite this facts in most of the literature, the authors suggest closure of the PDA, even in adult dogs, only important contraindication for not closing is right to left shunt.
It is not known why some animals with PDA do not show any signs until adulthood. One of the reasons could be the small diameter of the ductus. In human medicine the maintenance of normal pulmonary vascular resistance is important factor for survival of the older patients2. It is certain that the adult dogs with congenital heart diseases are more then we expect, and always when we examine adult animal for some heart disease, we have to think not only for degenerative valve disease and cardiomyopathies but also for congenital and inherited problems. And of course rare things do happen everyday.
Surgical extraction of adult D. immitis filariae from the pulmonary arteries of a patient with stage III heartworm disease
Ranko Georgiev1, Hristina Shukerova2, Nadezhda Petrova3(anesthetist)
1,2,3 DVM, Central Veterinary Clinic, Sofia, Bulgaria; 2016
An “exotic” diagnosis for Bulgaria just 5 years ago, Heartworm Disease (HWD) is a parasitic infestation that we nowadays see regularly in our small animal practice. Due to climate change and spreading of intermediate vectors, ever more dogs are getting affected. Other major contributing factors are the infrequency of preventive measures in the country and the high number of undiagnosed and subclinical patients, leading to a reservoir of hosts in the general canine population.
Rem is a 25kg, 10 years old MC mix breed dog admitted because of ascites and exercise intolerance during the past few weeks. Most prominent of the clinical signs was the severely distended, fluid-filled abdomen – assessed as modified transudate on abdominocenthesis (more than 4 liters were drained because of the labored breathing).
Thoracic X-rays revealed right-sided cardiomegaly and severely distended tortuous and blunt-ended pulmonary arteries. On echocardiography, right heart pathology was mainly observed – including a distended right atrium and ventricle, dilated pulmonary artery and evidence of pulmonary hypertension, as well as many tubular echoic structures in the lumen of the main pulmonary artery, typically identified as adult parasites.
Serology was positive for D. immitis (IDEXX 4D snap test) and the dog was classified as stage III HWD.
Because of the high worm burden and ascites, the possibility of interventional removal of the worms, before the adulticide treatment, was suggested to the owner, who gave his informed consent.
The patient was scheduled for surgery several days after hospitalization and treatment of right congestive heart failure and pulmonary hypertension using the following therapeutic protocol:
Torasemide: 0.2mg/kg/12h, IV and PO
Sildenafil: 2mg/kg/12h, PO
Ivermectin: 6ug/kg monthly, subcutaneously
Surgical extraction of worms was routinely performed using the right jugular vein approach. The area was scrubbed aseptically and a small skin incision was made over it. The vein was dissected free from the surrounding tissue and ligated proximally. A small transverse cut in its wall was made, through which a forceps was advanced into the heart under fluoroscopic control.
The anesthetic protocol we used was typical for this procedure; in particular premedication with Atropine, Butorphanol and Midazolam; induction with Etomidate; and finally Isoflurane maintenance.
After nearly 20 attempts, we extracted 25 adult worms. The overall fluoroscopic time of the procedure was less than 5 minutes. The recovery of the patient was uneventful and a day later we started the adulticide protocol for HWD treatment, as recommended by the American Heart Worm Association.
In all cases with stage III or IV HWD it is advisable to discuss the possibility of surgical extraction of some of the worms as a pre-adulticide step. This will lower the risk of fatal pulmonary thromboembolism after the injection of Immiticide and will likely improve the symptoms of existing pulmonary hypertension.
It should be noted that if a different extraction device is used (endoscopic loops and baskets, rigid or semi-rigid alligator forceps, different types of graspers, etc.), the success rate of the procedure is much lower, at least in our experience. The Ishihara forceps could be actively maneuvered into the RVOT, hence providing faster and easier access to the PA.
Surgical extraction of a heavy worm burden is possible and clinically important before adulticide treatment, in patients with end-stage HWD.
Rem, the dog of our study, successfully completed the treatment protocol for HWD without any evidence of pulmonary thromboembolism; meanwhile the symptoms of RCHF have slowly abated.
Pacemaker implantation (PMI) as treatment for AVB III and very slow ventricular escape rhythm in a geriatric canine patient
Ranko Georgiev1, Hristina Shukerova2, Nadezhda Petrova3
1,2,3 DVM, Central Veterinary Clinic, Sofia, Bulgaria
Pacemaker implantation is the most effective treatment for ‘syncope and severe exercise intolerance’ – related arrhythmias; however when searching for the best clinical decision for some older dogs, the risk of anesthesia often outweighs the benefits. We would like to share a case where the old age was not a problem.
Larry was a 17-year old MI mix breed dog admitted because of increasingly frequent exercise intolerance episodes during the past few months. Furthermore, the last week the patient was very week, unable to stand on his feet and with a depressed overall clinical status. On a clinical presentation with the referring vet а bradycardia was noted and the patient referred to us for a Cardiology consult.
During auscultation, a slow regular rhythm was detected with heart rate of 20 bpm classified as ventricular escape rhythm during the normal ECG. A 24hour Holter monitor revealed complete AV block (AVB III) throughout the study with an average rate of 31 bpm, occasional VE beats with some pairs, triplets and short runs; no pauses greater than 5 sec were noted. The slowest heart rate detected was 20 bpm.
Complete blood count and biochemical profile were normal. Radiography and echocardiography revealed generalized cardiomegaly, with mild-to-moderate mitral and tricuspid regurgitation and decreased contractility. During the abdominal FAST study a small amount of free fluid was noted – defined as a transudate on diagnostic abdominocenthesis. Lari_20150811163929_1640560
A diagnosis of complete AV block with clinical signs of right sided congestive heart failure was made and pacemaker implantation was decided. A VVI, bipolar, passive lead was fluoroscopically placed, under anesthesia, through the right jugular vein into the right ventricle, where it was successfully lodged.Lari_20150814181226_1819550 The lead was connected to a generator, which was later fixed in the subcutaneous tissue dorsally to the cervical vertebrae. A temporary pacemaker was used when the dog developed asystole during the procedure. Recovery from the surgery was uneventful, with the pacemaker capturing normally. The pacing rate was set to 100 bpm. The system used was a ‘St Jude’ one.
Our anesthesia protocol with this patient was routine for the procedure of a PMI – premedication with Midazolam and Buprenorphine, induction with Etomidate, intubation and maintenance with Isoflurane. The post procedure treatment was only with Cefazolin iv for the next few days.
The use of a temporary lead and/or an external pacemaker is highly advisable in patients who are depended on their escape rhythm.
Even though Larry recovered from the general anesthesia normally he was unable to stand on his feet for additional 5 days. He was bright, alert and responsive, with good appetite and normal consciousness, but with an impaired proprioception. We attributed this to the long period with severe bradycardia (HR of 20 bpm) and potential vasoconstriction/reperfusion complications. There is some data in the human medicine literature concerning PMI in old people with preexisting severe bradycardia, who reported pain in the extremities post the procedure.