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Introduo- cardiomiopatias

Cardiomiopatia dilatada em ces

OMS e da Federao Internacional de Cardiologia

Doena do miocrdio associada a disfuno cardaca (WHO/IFSC, 1996)

Classificao
Dilatada Hipertrfica Restritiva Arritmognica do VD

CESUMAR 2012

Mv. Msc. Arine Pellegrino

Definio- CMD
Doena miocrdica caracterizada por contratilidade reduzida e dilatao de um ou ambos os ventrculos

Etiologia
Base gentica/familiar
Boxer - autossmico dominante (MEURS, 1998) Doberman autossmico dominante (JVIM 2007; 21:1016-1020)

Deficincia de aas Primria

idioptica

Taurina Cocker Spaniel Carnitina Boxer

Fatores txicos Infeces Doenas imunemediadas Taquiarritmias Idioptica

Secundria
afeces que causam insuficincia miocrdica e dilatao ventricular

Prevalncia
Raas
Grandes a gigantes: Doberman, Boxer, Dogue Alemo, So Bernardo, Terra nova, Irish Wolfhounds, Dlmata Raas pequenas: Cocker Spaniel

Patofisiologia

Meia-idade/ jovens Sexo: > em machos Herana gentica (autossmica dominante)

Cocker, Boxer e Doberman

presso diastlica perfuso coronariana arritmias RVP Sobrecarga de volume remodelamento

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AE

AD

Patofisiologia
Desenvolvimento lento e prolongado choque cardiognco

PULMO

VE

VD

Aumento da presso diastlica final- congesto/ edema

CORPO

Hipertrofia excntrica Atrofia de msculos papilares Adelgaamento de parede e septo interventricular

CMD

Insuficincias valvares discretas a moderadas

Fases da CMD
Fase oculta
assintomtica

Fase oculta
Fase assintomtica Tempo de evoluo varivel (prolongado) Doberman
Arritmias ventriculares precedem alteraes ecocardiogrficas e manifestaes clnicas

Fase sintomtica
ICC

Boxer
Arritmias ventriculares

Diagnstico- Fase oculta

Holter 24h
> 50 VPCs/24 h (Boxer e Doberman)

Manifestaes clnicas
Cansao fcil Intolerncia a exerccios Apatia e prostrao/ letargia Tosse Dispnia e taquipnia volume abdominal- ascite Edema de membros Pr-sncope e sncope arritmias Caquexia Morte sbita

Ecocardiograma
ventricular e FS

Doberman (critrios de risco)

DVEd > 4,6 cm ou > 5,0 cm DVEs > 3,8 cm FS < 25% E-septo > 8mm

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Exame Fsico
Mucosas hipocoradas e TPC
Vasoconstrio perifrica e baixo DC

Exame fsico
Auscultao
Ritmo irregular (arritmias) Bulhas cardacas hipofonticas (efuses) Sopro sistlico discreto a moderado (insuficincias valvares secundrias) Ritmo de galope (S3)

Pulso: fraco, rpido e irregular Caquexia cardaca ICCE

Dispnia, taquipnia, tosse

ICCD
Pulso venoso jugular/ distenso jugular Hepato e esplenomegalia Efuses e edema de membros

CMD Doberman
Herana gentica Trs estgios:
Estgio I corao normal; sem manifestaes clnicas Estgio II (estgio oculto) corao anormal, sem manifestaes clnicas (arritmias podem estar presentes) Estgio III corao anormal; manifestaes clnicas ( ICC, sincope)

CM oculta/ Doberman
2 a 4 anos ICC, sincope ou morte sbita (primeira manifestao em 30% dos casos ) TV Critrios:
DVEd > 4,6 cm ou > 5,0 cm DVEs > 3,8 cm FS < 25% E-septo > 8mm 1 ou mais VPCs/min no ECG de repouso >50 VPCs no Holter; TV sustentada

CM Boxer
Boxer
Cardiomiopatia arritmognica do ventrculo direito Taquicardia ventricular Trs categorias:
1 assintomtico com VPCs ocasionais 2 sncope e intolerncia ao exerccio e arritmia ventricular 3 ICC, disfuno miocrdica, arritmias ventriculares

Alteraes laboratoriais
Azotemia pr-renal
perfuso renal

Aumento de enzimas hepticas

Congesto heptica

Hipoproteinemia
perfuso intestinal + caquexia

Alteraes histopatolgicas
Atrofia miofibrilar, fibrose e infiltrao por tec. Adiposo Miocitlise, necrose, hemorragia, infiltrado mononuclear

Hipercalemia e hiponatremia

OVERVIEW OF ELECTROCARDIOGRAPHY
THE NORMAL CARDIOVASCULAR SYSTEM
13
larger; the smaller septal (medial) leaflet lies close to the IVS in the area of the membranous septum. Generally,
5

53

8
1

there are three main papillary muscles, but their 47 episode of tachycardia. Episodes of tachycardia can be however, conduction backward (retrograde) into 2 6 number and configuration are variable . Inflow and outflow areas of the RV are separated by the muscular brief (paroxysmal) or prolonged (sustained). When the atria can cause a negative P wave after, supraventricular crest, so that the right AV and 7 3 semilunar valves are not adjacent as they are in the left 4 a premature complex follows each normal QRS, a semilunarsuperimposed even preceding the resulting 4 heart. The pulmonary valve is similar inon, or 8 appearance but thinner than the aortic valve (8). There 9 bigeminal pattern exists; the origin of the premature complex. are no coronary ostia QRS behind pulmonary valve cusps. 5 complexes determines whether the rhythm is SYSTEM The more general term supraventricular is used CONDUCTION 10 The sinoatrial (SA) node is the normal pacemaker of described as atrial or ventricular bigeminy. if it muscle is cells unclear whether the origin of ectopic the heart because the specialized here have 53 OVERVIEW OF ELECTROCARDIOGRAPHY the fastest intrinsic rate of automaticity (spontaneous complex(es) is 8atrial Canine heart: rightor ventricularjunctional. outflow tract. L = left; R = right; Clinically, diastolic depolarization). The SA node is located at the a = artery; v = vein. cranial aspect of the RA, near its junction with the 1. Aorta 2. Pulmonary (main pulmonary a.) 3. Pulmonary valve cranial vena cava. Electrical impulses originating from Supraventricular premature complexes distinguishing whether the trunk arrhythmia originates from 4. Supraventricular crest 5. R. ventricle 6. L. auricle 7. Great SA nodal cells spread into the RA, LA, and via the AV coronary v. (supraventricular) 8. Cranial interventricular branch of L. coronary a. in conduction the ventricles (9). Specialized These originate above the AV node, either in the system into above the AV node or below it cranial (paraconal) interventricular groove 9. Tricuspid valve fibers (internodal pathways) facilitate conduction 10. L. ventricle important. the RA and LA to the AV node. atria or the AV junctional area. Because through their (ventricular) is most Supraventricular GENERAL PRINCIPLES ECG LEAD SYSTEMS f tachycardia can be however, conduction backward (retrograde) Several standard leads are used node to evaluate cardiac conduction into and through into the ventricles occurs premature activity usually depolarizes the sinus The electrocardiogram (ECG) records the electrical electrical activity (Table 8, p. 48). The orientation of a (sustained). When the atria can cause negative wave after, via a the normal P conduction pathway, their QRS as well. This the sinus lead rhythm creates a activity (depolarization andresets repolarization) of cardiac with respectand to the 9 heart is called the lead axis. A muscle from the body surface and provides information lead records the depolarization and repolarization configuration is normal an intraventricular noncompensatory pause (i.e. waves thethat interval between ch normal QRS, a superimposed on, or even preceding the (unless resulting on heart rate, rhythm, and intracardiac conduction. are aligned with it. If the direction of Ao also suggest the presence of specific ECG findings may myocardial activation parallels the lead axis, a conduction disturbance or enlargement is also the complexes and following the in of the premature QRS complex. chamber sinus enlargement, myocardial disease, preceding ischemia, Sinus node relatively large deflection will be recorded. As the angle pericardial disease, certain electrolyte imbalances, and between the lead axis and the direction of the activation muscle present). Premature complexes that arise within Atrial the premature complex than that three r the rhythm is The more general term supraventricular is used some drug toxicities. However, the ECG is does less not wave increases (up to 90 of degrees), the ECG deflection (1.01.2) Atrium record cardiac mechanical activity; therefore, the ECG that lead becomes smaller. The ECG deflection is atria (i.e. the outside the SA are usually preceded consecutive sinus complexes). in bigeminy. if it is unclear whether origin of node) ectopic by itself cannot be used isoelectric when the activation wave is perpendicular to LA to diagnose congestive heart Sinus node failure, assess the strength (or even presence) of cardiac the lead axis. Each lead has a positive and a negative by an P wave (positive, negative, or RA contractions, or predict whether the patient will survive complex(es) is atrial or abnormal junctional. Clinically, AV node AV node pole or direction. A positive ECG deflection will be anesthetic or surgical procedures. recorded if the cardiac activation wave moves toward (0.020.1) Atrial tachycardia biphasic configuration) called a P wave (7982 ). This chapter reviews basic guidelines for the positive pole (electrode) of the lead. If the wave of exes distinguishing whether the arrhythmia originates from Bundle of His Variveis (1.22.0) ECG acquisition, interpretation, originates and ambulatory from an abnormal atrial Atrial tachycardia Sometimes, the premature impulse is conducted C ARDIOVASCULAR ISEASE INabove SMALL the ANIMAL EDICINE Bundle of His LV monitoring. node, either inDthe AV M node (supraventricular) or below it RV ECG features typical of specific diseases are discussed or more fully in the chapters describing those focus atrial reentry (repetitive activation from69 slowly (prolonged PQ interval) or with a bundle Purkinje fibers Right Aumento de is trio e/ou ventrculos conditions. Approaches to managing abnormal cardiac Ventricle bundle branch rea. Because their (ventricular) most important. Supraventricular (2.04.0) electrical an abnormal circuit branch block pattern. If an ectopic P wave occurs rhythms are found conduction in Chapter 17. Other around means of evaluating cardiac electrical activity, such as intrae ventricles occurs premature activity usually depolarizes the sinus node QRS Arritmias within the, atria). P (signal waves are often hidden within the before the AV node has completely repolarized, the high resolution averaged) cardiac recording ECG , and heart rate variability (HRV) analysis are thway, their QRS as well. This resets impulse thegigantes sinus rhythm and creates a the ventricles ECG Purkinje fibers QRS-T Atrial tachycardia is usually a may not be conducted into (an FA: 75 a 80% das raas not discussed complexes. here (see references for more 1 r What is an ECG? (2.04.0) egular QRS intervals Atrial flutter R information). Ventricular muscle an intraventricular noncompensatory pause (i.e. the interval between regular rhythm unless the exceeds the AV nodes example of physiologic AV block). Junctional (0.31.0) The normal cardiac rhythm originates in rate the Dobermans e Boxers: arritmias ventriculares f atrial to ventricular Atrial flutter results from a single (macro-) reentrant sinoatrial (SA) node and follows the cardiac Left bundle branch conduction largement is also the sinus complexes preceding following the by a P wave; ability to conduct every complexes areand usually not preceded (2.04.0) 9 (p. pathway illustrated in figure 13). ECGimpulse, in which case

Overview of Electrocardiography

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Alteraes eletrocardiogrficas

P1: FAW/FFX

P2: FAW/FFX

QC: FAW/FFX 16:33

T1: FAW

BLUK114-Martin

August 4, 2007

1 r What is an ECG?

36

pic P wave occurs ely repolarized, the ycardia to the ventricles (an ay involve a reentrant block). Junctional node. This can occur ded by a P wave; of slow- and fastode, or by means of an 16, 17. A premature mpulse can initiate such ed by impulses looping V node or the AV node mals with ventricular 79 pisodes of reentrant n normalize or prolong P waves, and normalunless a simultaneion disturbance is a eventually leads to

duction) the hat arise preserves within the If usually atrial tachycardia re preceded tricular conduction, itive, negative, or ckPpattern ECG, wave (on 7982 ). r tachycardia can be pulse is conducted rdia dogs have or in with a may bundle

wave of electrical activation cycling premature complex is lessregularly than that of through three Holter usually at >300400 cycles/minute. The the atria16,sinus consecutive complexes). Boxer: > 100 VPCs/24 hs depends on AV conduction ventricular response rate Exames seriados and may be irregular or regular. Sawtooth flutter Atrial tachycardia waves, representing recurrent atrial activation, are seen Atrial tachycardia originates from an abnormal atrial between complexes the ECG activation (86). Atrial flutter focus or QRS atrial reentry on (repetitive from is not a stable rhythm; it often an degenerates into atrial electrical conduction around abnormal circuit fibrillation (AF)P but may convert to sinus rhythm. within the atria). waves are often hidden within the Atrial enlargement a common underlying factor. a QRS-T complexes. is Atrial tachycardia is usually
P1 P1

An electrocardiograph (ECG), in its simplest form, is a voltmeter (or galvanometer) that records the changing electrical activity in the heart by means of positive and negative electrodes (Fig. 1.1). Elec- P-QRS-T (69), are generated as the heart waveforms, e v trocardiography is the9 process of recording these changing potential Cardiac conduction system. Major components of the cardiac system are indicated on the left, with approximate conduction speed muscle is depolarized and conduction then repolarized (see Chapter differences. P (m/sec) in parentheses. On the right, representative action potentials are colorrepresents coded to the conduction system components. A composite ECG 1). QRS complex as a whole electrical While a positive (+ve) and negative (ve) electrode canThe be placed (below) illustrates the electrical activation sequence structures. almost anywhere on, or in, the body to record changes, oneof activation ofthese ventricular muscle, regardless of whether of the most common and simplest methods is to place these electrodes individual Q, R, or S components, or variations on the limbs of the animal referred to as a body surface limb thereof, are present or absent. The configuration of the ECG recording. In comparison, for example, electrodes can be placed on the chest (precordial chest ECG recording commonly used in QRS complexes depends on the lead recorded as well as PR humans) or inside the cardiac chambers (used in electrophysiological the electrical activation pattern of the ventricles; there is (PQ) studies). This book is conned to the limb ECG recording, which is Figure 1.1 An ECG records the hearts electricity. some variation from animal to animal. Table 7 (p. 48) the method most commonly used in veterinary medicine.
+v e

Ware, W., 2007

QT

summarizes the events underlying ECG waveforms and time intervals.

79

69 P-QRS-T from a dog. Lead II at 50 mm/sec, 1 cm = 1 mV. Waveforms and intervals are indicated. Each small box is 0.02 seconds in duration (X axis) and 0.1 mV in amplitude (Y axis).

80

regular rhythm unless the rate exceeds the AV nodes Atrial fibrillation ability to conduct every impulse, in which case Atrial electrical activation is rapid and chaotic because Martin, of multiple small reentrant circuits in AF16. The AV M., TAQUIARRITMIAS TAQUIARRITMIAS 2007 node is bombarded by these chaotic electrical impulses; SUPRAVENTRICULARES SUPRAVENTRICULARES therefore, AV conduction velocity and recovery time 79, 80 Examples of premature supraventricular ectopic activity. (79) Atrial bigeminy in a 6-year-old female Irish Wolfhound several days after determine the (ventricular) heart rate. No P waves are surgery for gastric dilatation-volvulus. Note the notched negative P waves. (80) Junctional premature complex in an older male Doberman Pinscher. seen on ECG because no uniform atrial depolarization FC alta (360 bpm) wave occurs. The ECG baseline usually shows irregular Ritmo regular "Ausncia de ondas P undulations known as fibrillation (f) waves 80 (87, 88). Because organized electrical activity is absent, effective 81 82 atrial contraction is lacking. AF causes an irregular heart rhythm, usually with a rapid rate. Heart rate in patients with AF should be monitored using the ECG because heart rate estimation by auscultation can be highly inaccurate20. Most often the QRS complexes are

Complexo atrial prematuro- APC

Taquicardia atrial- TA

ular ectopic activity. (79) Atrial several days after 84bigeminy in a 6-year-old female Irish Wolfhound85 285 MYOCARDIAL DISEASES OF THE DOG the notched negative P waves. (80) Junctional premature complex in an older male Doberman Pinscher. P P Ware, W., 2007 81, 82 (81) Paroxysm of supraventricular tachycardia (bracket) in an old Siamese cat. (82) Sustained supraventricular tachycardia at Ware, a rateW., of 2007 P
360 beats/minute in a Labrador Retriever puppy common with mitral and valve dysplasia. All examples are lead IIventricular at 25 mm/sec, 1 cm = 1with mV. sinus (418 ). Atricuspid bundle branch block pattern or paroxysmal tachycardia,

81

82

other intraventricular conduction disturbance is sometimes seen. In dogs with sinus rhythm, P waves are often widened and notched (suggesting LA enlargement). AF is quite common (419, 420; also 87, p. 54), especially in Great Danes and other giant breeds 2, 19. Uniform or multiform VPCs and

rhythm or AF, are typical in Doberman Pinschers and Boxers and are also seen frequently in other breeds (421, 422; also 91, 94, and 99, p. 5557). Echocardiography is the best clinical means for assessing cardiac function and chamber size, and for excluding other acquired or congenital cardiac disease.

f 200 beats/minute in an 11-year-old Yorkshire Terrier. Note the negative P waves, one ofTAQUIARRITMIAS which is not 418-420 (418) Sinus tachycardia in a 9-year-old female Doberman SUPRAVENTRICULARES 1 cm = 1 mV. (84) Wide-complex supraventicular tachycardia in a male Irish Wolfhound with Pinscher with DCM and pulmonary asily mistaken for ventricular-origin tachycardia. (85) Sinus rhythm in the dog in 84. Examples 84 and edema. The wide P waves are consistent with LA enlargement; mV. wide QRS complexes with slowed

418

419

420

Fibrilao atrial- FA

chycardia (bracket) in an old Siamese cat. (82) Sustained supraventricular tachycardia at a rate of 87 ppy with mitral and tricuspid valve dysplasia. All examples are lead II at 25 mm/sec, 1 cm = 1 mV.

FC alta (200 bpm) and sloppy R wave descent Ritmo irregular suggest myocardial disease with slowed intraventricular conduction. Ausncia de ondas P

Leads as marked; 50 mm/sec, 1 cm = 1 mV. (419) AF with uncontrolled ventricular response rate (~230 beats/minute) in a 3-year-old male Doberman Pinscher with severe signs of heart failure from DCM. (420) ECG from the same dog as in 419 one month later when signs of congestion were absent. The ventricular rate is well controlled (110 beats/minute); baseline fibrillation waves are clearly evident now. 419, 420: leads as marked; 25 mm/sec, 1 cm = 1 mV.

man Shorthaired Pointer ter waves at a rate of about 1 mV.

87 Atrial fibrillation with an uncontrolled ventricular rate of W., 2007 Ware, 220/minute in a 4-year-old male Labrador Retriever with DCM. Note the irregular R to R intervals and small f waves in the baseline. Lead II at 25 mm/sec, 0.5 cm = 1 mV.

WARE, 2007 421

422

(422) Frequent VPCs, as pairs and triplets, in a 9-year-old female Doberman Pinscher with DCM and clinical heart failure. (422) Multiform VPCs in a 5-year-old male Labrador Retriever with DCM. The QRS compexes are quite small, but no effusion or other cause was evident. The P waves are wide. 421, 422 Leads as marked; 25 mm/sec, 1 cm = 1 mV.

common (418). A bundle branch block pattern or other intraventricular conduction disturbance is sometimes seen. In dogs with sinus rhythm, P waves are often widened and notched (suggesting LA enlargement). AF is quite common (419, 420; also 87, p. 54), especially in Great Danes and other giant breeds 2, 19. Uniform or multiform VPCs and
418-420 (418) Sinus tachycardia in a 9-year-old female Doberman Pinscher with DCM and pulmonary edema. The wide P waves are consistent with LA enlargement; wide QRS complexes with slowed and sloppy R wave descent suggest myocardial disease with slowed intraventricular conduction. Leads as marked; 50 mm/sec, 1 cm = 1 mV. (419) AF with uncontrolled ventricular response rate (~230 beats/minute) in a 3-year-old male Doberman Pinscher with severe signs of heart failure from DCM. (420) ECG from the same dog as in 419 one month later when signs of congestion were absent. The ventricular rate is well controlled (110 beats/minute); baseline fibrillation waves are clearly evident now. 419, 420: leads as marked; 25 mm/sec, 1 cm = 1 mV.

paroxysmal ventricular tachycardia, with sinus rhythm or AF, are typical in Doberman Pinschers and Boxers and are also seen frequently in other breeds (421, 422; also 91, 94, and 99, p. 5557). Echocardiography is the best clinical means for assessing cardiac function and chamber size, and for excluding other acquired or congenital cardiac disease.

286

CARDIOVASCULAR DISEASE IN SMALL ANIMAL MEDICINE

418

419

420

286

421

422

parasternal 4-chamber view usually provides long-axis Aumento de AE (Boxer e Doberman) a view with maximal LV dimensions, although the left apical view is better some dogs. LV volumes in Edema e in congesto pulmonar 423 424 diastole and systole (from 2-D images) and EF can then 2 Efuso pleural, pericrdica ascite (10 . Averages from 5 cardiace cycles be calculated RV cycles, if AF is present) obtained from the view
(422) Frequent VPCs, as pairs and triplets, in a 9-year-old female Doberman Pinscher with DCM and clinical heart failure. (422) Multiform VPCs in a 5-year-old male Labrador Retriever with DCM. The QRS compexes are quite small, but no effusion or other cause was evident. The P waves are wide. 421, 422 Leads as marked; 25 mm/sec, 1 cm = 1 mV.

Dilated and rounded cardiac chambers, poor systolic ventricular wall and septal motion, reduced FS CARDIOVASCULAR DISEASE IN (<2025%) and ejection fraction (EF; <40%), and increased mitral EPSS (>6 mm) are characteristic findings (423425; also 148, 149, pp. 79, 80). All chambers are usually affected, but the right heart may Dilated andrelatively rounded cardiac systolic appear normal, chambers, especially poor in Doberman ventricular septal reduced FS Pinscherswall and and Boxers. LV motion, free wall and septal (<2025%) and fraction (EF; <40%), and thicknesses areejection normal to decreased. Mild to moderate increased mitral EPSS (>6 mm) are characteristic AV valve regurgitation may be evident with Doppler (426, (427 ). Maximum LV dimensions M-mode findings 423425 ; also 148, 149, pp. (from 79, 80). All or 2D) should compared with breed-specific chambers are usuallybe affected, but the right heart may normals when possible (see Table 16 , p. 72); a cut-off appear relatively normal, especially in Doberman value for LV enlargement two wall standard Pinschers and Boxers. LV of free anddeviations septal above mean reference value has been until thicknesses are normal to decreased. Mild proposed to moderate 2. The right specific information available AV more valve regurgitation may be is evident with Doppler parasternal long-axisLV 4-chamber view usually provides (426, 427). Maximum dimensions (from M-mode viewshould with maximal LV dimensions, the left or a 2D) be compared with although breed-specific apical view is better in some dogs. LV volumes normals when possible (see Table 16, p. 72); a cut-offin diastole and systole (from images) anddeviations EF can then value for LV enlargement of2-D two standard 2. Averages from 5 cardiac cycles (10 be mean calculated above reference value has been proposed until Cardiomegalia cycles, if AF is present)is obtained the view 2. The right more specific information availablefrom

recommended . LV end-diastolic and en SMALL ANIMAL MEDICINE volumes are normalized to body surfac

showing

maximal
2

LV

dimensions

ha

Alteraes radiogrficas

yield end-diastolic and end-systolic volum (EDVI and ESVI, respectively; see Chapter Dogs with overt DCM generally have an showing LV dimensions ha LV spheri over 80 maximal ml/m2. Increased recommended end-diastolic en characteristic2.ofLV DCM; an index and of sp volumes are normalized body proposed to quantify this to (Table 58,surfac p. 28 yield end-diastolic end-systolic volum <1.65 are thought and to represent increased Otherand cardiac or systemic (EDVI ESVI, respectively; seedisease, Chapter hypertension, must be excluded to have make an ad Dogs with overt DCM generally primary DCM. Diastolic fu LV spheric over 80 (idiopathic) ml/m2. Increased thought to deteriorate only after overt DCM characteristic of DCM; an index of sp A restrictive transmitral pattern and proposed to quantify thisfilling (Table 58, p. 28 E wave have been corre <1.65 aredeceleration thought to time represent increased increased LV diastolic pressure and poor pr Other cardiac or systemic disease, people. Preliminary evidence (restrictive mit hypertension, must be excluded to make a di pattern and E wave deceleration <80 m/sec primary (idiopathic) DCM. Diastolic fu 49. the same in dogs thought to deteriorate only after overt DCM A restrictive transmitral filling pattern and E wave deceleration time have been corre increased LV diastolic pressure and poor pr people. Preliminary evidence (restrictive mit pattern and E wave 425 deceleration <80 m/sec the same in dogs49.

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RV

RV IVS

Distenso da veia cava

423
WARE, 2007

LV Hepato e esplenomegalia

LV

424
RV

425
LV

RV

RV IVS

LV LV 423-425 2-D echo images of the LV at end-diastole (423) and maximal systole (424) show little change in ventricular size in a 4-yea Labrador Retriever with heart failure from DCM. Right parasternal short-axis view. (425) M-mode LV image of the LV from a 7-year-old Dalmation shows abysmally poor septal and LV free wall motion as well as biventricular dilation. LV = left ventricle; RV = right ventri IVS = interventricular septum.

Alteraes ecocardiogrficas
Melhor meio para diagnstico Dilatao das cavidades DVEs- (fase oculta) da frao de encurtamento (<25%)
142

da de ejeo (< SECTION II frao Cardiovascular Disease

40%)

Figure 7-2. rhythm, lack of P waves, and widened QRS complex. 50 mm/sec; 10 should mm/mV. or 2D) be compared with breed-specific normals when possible (see Table 16, p. 72); a cut-off value for LV enlargement of two standard deviations above mean reference value has been proposed until more specific information is available2. The right parasternal long-axis 4-chamber view usually provides a view with maximal LV dimensions, although the left apical view is better in some dogs. LV volumes in diastole and systole (from 2-D images) and EF can then be calculated2. Averages from 5 cardiac cycles (10 cycles, if AF is present) obtained from the view

Dogs with overt DCM generally have an ESVI well over 80 ml/m2. Increased LV sphericity is a characteristic of DCM; an index of sphericity is Pinschers and Boxers. LV free wall and septal Mitral valve E-point to septal separation (EPSS) = distance to quantify this (Table 58, p. 282). Values thicknesses are normal to decreased. Mild to moderate between maximal mitral proposed opening in early diastole (E point LVIDd <1.65 surface are thought to represent increased sphericity. AV valve regurgitation may be evidenton with Doppler M-mode) and endocardial of interventricular Dilated and rounded cardiac chambers, poor systolic showing maximal LV dimensions have been septum M-mode Other cardiac or systemic disease, including (426, measurements 427). Maximum dimensions (from 2. LV 2007 (LV internal dimension taken LV at chordal ventricular wall and septal motion, reduced FS recommendedWARE, end-diastolic and end-systolic hypertension, must be excluded to make a diagnosis of or 2D) should be compared with breed-specific level) Mean velocity of circumferential fiber shortening (Vcf) volumes are normalized to normals body when surface area to (<2025%) and ejection fraction (EF; <40%), and primary (idiopathic) DCM. Diastolic function is possible (see Table 16, p. 72); a cut-off LVIDs End-systolic index (ESVI) = enlargement ESV increased mitral EPSS (>6 mm) are characteristic yield end-diastolic and volume end-systolic volume indices thought to deteriorate only after overt DCM develops. value for LV of two standard deviations = LVIDd LVIDd LVET transmitral filling pattern and shortened BSA 5, p. value A restrictive above mean reference (EDVI and ESVI, respectively; see Chapter 79). has been proposed until findings (423425; also 148, 149, pp. 79, 80). All Theis right E the wave deceleration time have been correlated with more have specific derived from time between aortic valve chambers are usually affected, but the right heart may Dogs with overt DCM generally an information ESVI well is available2.(LVET ESV derived from 2-D: opening and closing increased on M-mode, ordiastolic the duration of parasternal long-axis 4-chamber view usually provides LV pressure and poor prognosis in 2 over 80 ml/m . Increased LV sphericity is a appear relatively normal, especially in Doberman aortic the flowleft signal on people. Doppler examination) a view with maximal LV dimensions, although Preliminary evidence (restrictive mitral inflow Short-axis area/long-axis length = 5AL characteristic of DCM; an apical indexview of is sphericity is Pinschers and Boxers. LV free wall and septal better in some dogs. LV Vvolumes infor heart pattern and E wave deceleration <80 m/sec) suggests normalized rate = (LVIDd LVIDs) 100 cf 6 proposed to quantify this (Table 58and , p.systole 282).(from Values thicknesses are normal to decreased. Mild to moderate diastole 2-D images) and EF can then the same in dogs49. (LVIDd LVET HR) <1.65 are thoughtLong-axis to represent increased sphericity. AV valve regurgitation may be evident with Doppler area length = 8A2 2. Averages from 5 cardiac cycles (10 be calculated Lead II ECG tracing from a dog indicating atrial brillation and left ventricular enlargement. Note the irregular LV freethe wall view thickening (%FWth) = LVFWs LVFWd 100 cycles, if present) obtained from Other cardiac or systemic disease, (426, 427). Maximum LV dimensions (from M-mode 3 L AF is including
Table 17 Selected echocardiographic measures of LV especially systolic function. appear relatively normal, in Doberman Fractional shortening (FS) = LVIDd LVIDs 100

286 ou adelgaados Parede VE e SIV normais

426, 427 (426) Color flow Dopp illustrates mild MR in an 8-year-o Doberman Pinschersize with an 423-425 2-D echo images RV of the LV at end-diastole (423) and maximal systole (424) show little change in ventricular inDCM a 4-yea chambers dilated. (427) Mild Labrador Retriever with heart failure from DCM. Right parasternal short-axis view. (425) M-mode image of the are LV from a 7-year-old RA in the same Right pa Dalmation shows abysmally poor septal and LV free wall motion as well as biventricular dilation. LV =evident left ventricle; RV =dog. right ventri long-axis view. LA = left atrium; L IVS = interventricular LV septum. ventricle; RA = right atrium; RV = ventricle. 426, 427 (426) Color flow Dopp 426 427 LA illustrates mild MR in an 8-year-o Doberman Pinscher with DCM and 286 RV CARDIOVASCULAR DISEASE IN SMALL ANIMAL MEDICINE chambers are dilated. (427) Mild RA evident in the same dog. Right pa Dilated and rounded cardiac chambers, poor systolic showing maximal LV dimensions have view. beenLA = left atrium; L long-axis 2. LV end-diastolic and end-systolic LV ventricular wall and septal motion, reduced FS recommended 80 CARDIOVASCULAR DISEASE IN SMALL ANIMAL MEDICINE ventricle; RA = volumes are normalized to body surface area toright atrium; RV = (<2025%) and ejection fraction (EF; <40%), and increased mitral EPSS (>6 mm) are characteristic yield end-diastolic and end-systolic volume indices ventricle. (EDVI and ESVI, respectively; see Chapter 5, p. 79). findings (423425 LA ; also 148, 149, pp. 79, 80). All CARDIOVASCULAR DISEASE IN SMALL ANIMAL MEDICINE
chambers are usually affected, but the right heart may

426

427

hypertension, mustModified be excluded to make a diagnosis Simpsons Rule (Method of Disks) = of primary (idiopathic) DCM. Diastolic function is n r2 x L after thought to deteriorate only overt DCM develops. 423 n i=1 A restrictive transmitral filling pattern and shortened (based on dividing LV along its long axis into a series E wave deceleration time havethe been correlated with RV of disks of equal thickness) increased LV diastolic pressure and poor prognosis in people. Preliminary evidence (restrictive mitral inflow LV pattern and E wave deceleration <80 m/sec) suggests the same in dogs49.

LVFWd

425 424 length; LVET = left ventricular ejection time; LVIDd = left

A = left ventricular area; BSA = body surface area (m2); ESV = end-systolic volume; HR = heart rate; L = left ventricular ventricular internal dimension at end-diastole; LVIDs = left ventricular internal dimension in systole; LVFWd = left RV ventricular free wall thickness in diastole; RV LVFWs = left ventricular free wall thickness in systole; n = number of IVS disks; r = disk radius.
LV LV

Systolic time intervals (see p. 82) and mitral annular motion32 are other methods of assessing LV function.

Figure 7-3. pathy. Note

As disease progresses from occult to overt, echocardiography helps monitor heart enlarge426 ment, assess contractility, and evaluate secondary mitral regurgitation. Echocardiography is used in conjunction with chest radiographs to help decide when to initiate therapy. Common echocardiographic ndings in dogs with advanced occult or overt clinical disease include the following: Moderate to severe left ventricular and atrial enlargement (Figure 7-3). Reduced systolic motion of the left ventricular wall and interventricular septum (Figure 7-4). Mild to moderate mitral regurgitation secondary to mitral annulus dilation. Incomplete systolic opening of the aortic valves.

423-425 2-D echo images of the LV at end-diastole (423) and maximal systole (424) show little change in ventricular size in a 4-year-old male Mitral valve motion is also evaluated using M-mode. 425 Labrador Retriever with heart failure from The anterior (septal) leaflet is most prominent and hasDCM. Right 149parasternal short-axis view. (425) M-mode image of the LV from a 7-year-old female an M configuration. The motion of poor the septal smaller Dalmation shows abysmally and LV free wall motion as well as biventricular dilation. LV = left ventricle; RV = right ventricle; posterior (parietal) leaflet appears as a W, and is IVS = interventricular septum. RV RV RV RV more easily seen in the dilated ventricle. Tricuspid valve 426, 427 (426) Color flow Doppler image 426is similar. The leaflet motion 427 IVS leaflet motion pattern is identified by letters (140, p. 77). Point E is 1VS illustrates mild MR in an 8-year-old female the maximal opening of the valve during rapid Doberman Pinscher with DCM and AF. All the RV LV LV ventricular filling. In normal animals the mitral E chambers are dilated. (427) Mild TR is also LV point lies close to the IVS. Poor myocardial RA evident in the same dog. Right parasternal contractility is the most common cause of an LV M long-axis view. LA = left atrium; LV = left increased E point to septal separation (EPSS; 149). LV ventricle; RA = right atrium; RV = right Normal EPSS is generally considered )6 mm in dogs, ventricle. although it may be greater in giant breed dogs27, and LA 4 or 5 mm in cats7. Atrial contraction opens the valve LVW to point A. Normally, leaflet excursion is greater at point E. With tachycardia, the A point merges with 2-dimensional echocardiogram of the left ventricle (LV) and atrium (LA) of a Great Dane with dilated cardiomyoWARE, 2007 WARE, 2007 149 This M-mode echo from a Labrador Retriever with dilated E point; this is common cats (150, 151 ). 2-D echo images of the LV at end-diastole (423) and maximal systole (424) show littlethe change in ventricular size in in a 4-year-old male the dilated ventricular and atrial chambers. RV,423-425 Right ventricle; RA, right atrium. cardiomyopathy shows marked LV dilation, poor IVS and LVW motion, Dynamic LV outflow obstruction causes the Labrador Retriever with heart failure from DCM. Right parasternal short-axis view. (425) M-mode image of the LV fromto a be 7-year-old female the septum and wide E point to septal separation (29 mm). RV = right ventricle; anterior mitral leaflet sucked toward Dalmation shows abysmally poor septal and LV free wall motion as well as biventricular dilation. during LV = left ventricle; RVis=called right ventricle; IVS = interventricular septum; LV = left ventricle; LVW = left ejection. This systolic anterior motion ventricular free wall; M = mitral valve. (SAM). SAM causes the normally straight anterior leaflet IVS = interventricular septum.

Mitral valve

echos (between points C and D) to bend toward the septum during systole (152, 153). Diastolic flutter of the anterior mitral leaflet is seen sometimes when an aortic insufficiency jet causes the leaflet to vibrate (154156).

423

424

Decreased systolic thickening of the left ventricular wall and interventricular septum. The echocardiogram in427 Boxers with ARVC is usually normal. Subtle right ventricular dilation RV or wall motion abnormalities may be noted.
RA

LV Concomitant Abnormalities in Moderate or Severe Dilated LA Cardiomyopathy

426, 427 (426) Color flow Doppler image illustrates mild MR in an 8-year-old female Doberman Pinscher with DCM and AF. All the chambers are dilated. (427) Mild TR is also evident in the same dog. Right parasternal long-axis view. LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.

Azotemia is commonly detected in dogs that are receiving diuretic therapy and is typically prerenal in nature. Mild azotemia (blood urea nitrogen < 60 mg/ dl and creatinine < 2.5 mg/dl) usually does not require specic treatment or cessation or reduction of diuretic therapy. More severe azotemia (blood urea nitrogen

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Diagnstico- CMD oculta

Critrios maiores (valor: 3 pontos)
sistlico e diastlico do VE da frao de encurtamento: <20-25% da frao de ejeo: <40% da esfericidade : <1,65

Tratamento- objetivos
manifestaes da ICC Dbito cardaco Manejo e controle de arritmias Melhorar a qualidade de vida

Critrios menores (valor: 1 ponto) Holter (Boxer e Doberman)

Mais de 50 VPCs em 24 horas

Fibrilao atrial Distncia E-septo > 0,8 cm PEP/TEVE > 0,4 FS entre 25 e 30% do AE ou AE e AD

Diagnstico: > 6 pontos

a sobrevida

Tratamento- fase oculta

iECA (remodelamento e controle neuro-humoral)

Tratamento- fase sintomtica

Vasodilatadores
iECA

Inotrpicos positivos
Pimobendan e digoxina

Antiarrtmicos (quando necessrio)

Sotalol (arritmias ventriculares) Amiodarona (arritmias ventriculares e supraventriculares) Diltiazem (arritmias supraventriculares)

Diurticos
Furosemida, espironolactona e hidrocortiazida

B-bloqueadores
carvedilol

Suplementos
Omega 3, L- carnitina e taurina

Presso arterial

Vasodilatadores
iECA (prils)
Benazepril- 0,25 a 0,5 mg/Kg SID a BID
Metabolizao heptica e renal

Perfuso renal ( Na) Renina Angiotensinognio Angiotensina I

Inibidores da ECA ECA ANGIOTENSINA II Sede Norepinefrina Remodelamento Aldosterona Radicais livres Sdio H2O !!! ADH Vasoconstrio

Enalapril- 0,25 a 0,5 mg/Kg BID

Metabolizao renal

Lisinopril- 0,25 a 0,5 mg/Kg SID a BID

Metablito ativo

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Diurticos
n Quando h sinais de congesto n Furosemida
n 2 a 4 mg/Kg SID a TID n perda de K n diurtico de ala n 2 a 4 mg/Kg SID a BID n inibidor da aldosterona- efeito cardio-protetor n 2 a 4 mg/Kg BID n perda de K n Ao tubular

Inotrpicos positivos
Digoxina
0,003 a 0,005 mg/Kg BID 0,22mg/m2 BID (caes > 20Kg) Ao sobre Na/K ATPase Aumenta disponibilidade de clcio ( inotropismo) tnus parassimptico / tnus simptico ( FC) Dosagem srica- controle do nvel teraputico Efeitos colaterais: diarria, vmitos, anorexia, arritmias Cuidados: doena renal, anorexia, hipocaliemia

n Espironolactona

n Hidroclortiazida

n Associaes- bloqueio sequencial do nfron

Inotrpicos positivos- Pimobendam

Ao
Inibidor da fosfodiesterase do tipo III Sensibilizador de Ca++ Menor consumo oxignio pelo miocrdio

Pimobendam na ICC
Melhora prognstico (risco cardaco)
Smith et al., J Small Anim Practice, 46, 121-30, 2005 (melhor prognstico)

Melhora classe funcional

Lombard et al., J Am Anim Hosp Assoc., 42, v.4, 249-61, 2006 Kanno et al., J Vet Med Sci, 69, 4, 373-7, 2007

Dose- 0,1 a 0,3 mg/Kg BID (jejum) Efeitos:

Inotrpico positivo e vasodilatador ( ps-carga) Lusitrpico positivo Reduo citocinas inflamatrias

Aumento no tempo de vida

Lombard et al., J Am Anim Hosp Assoc., 42, v.4, 249-61, 2006

Melhora contratilidade (assintomticos)

Chetboul et al., J Vet Int Med, 21, 4, 742-53, 2007

Cardioprotetores"
Beta-bloqueadores- carvedilol
Diminui ao catecolaminas no miocrdio Anti-oxidante (reduo radicais livres) Vasodilatador (bloqueador alfa1) Dose: 0,3 0,8 mg/kg/BID (ajuste gradual)

Taurina e carnitina
Cocker Spaniel - taurina e carnitina Boxer carnitina Manter terapia convencional at melhora significante na funo miocrdica (eco) 4 a 6 meses Retirar gradualmente: digoxina, iECA e diurticos Monitorar manifestaes clnicas FC e FR

Espironolactona
Antagonista da aldosterona

mega 3 e 6
Indicados para minimizar caquexia Inibio de canais de sdio voltagem-dependentes

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Taurina e carnitina
Doses
Taurina: Ces < 25 kg: 500 a 1000 mg, com alimento, TID Ces > 25 kg: 1 a 2 g, com alimento, BID ou TID Carnitina: Ces < 25 kg: 1g com alimento TID Ces > 25 kg: 1-2 g, com alimento TID

Antiarrtmicos
SOTALOL
Atividade classe II e III
efeito classe III + efeito -bloqueador

Indicaes

Arritmias ventriculares previne MS (pela FV) CMO Boxer (Cardiomiopatia Arritmognica do VD) inotrpico negativo durao do potencial de ao TORSADES DE POINTES

Toxicidade

Dose

co: 0,5-2,0 mg/kg BID VO

Antiarrtmicos
AMIODARONA Atividade classe I, II, III e IV Indicaes taquicardias supra e ventriculares agudas e crnicas Toxicidade (incidncia desconhecida em ces) GI e hepatopatias, fibrose pulmonar, neutropenia e alteraes da tiride n. sricos de digoxina, quinidina, procainamida hipotenso quando IV Dose VO: 10-15 mg/kg BID 7 dias; aps 5-7,5 mg/kg BID 7 dias; aps SID IV: 5-10 mg/kg (bolus bem lento)

Prognstico
Reservado a mau Doberman
Aproximadamente 3 meses de sobrevida 20% a 40%- morte sbita antes de ICC

25% a 40%- sobrevida > 6 meses (qdo tem boa resposta ao tratamento inicial) 7,5% a 28%- sobrevida de 2 anos

Concluses
Fase oculta Fase sintomtica Raas predispostas
Variaes de acordo com o padro racial

Prognstico reservado a mau