an introductory guide

1. (Role of electrocardiography in
animals
And
A introductory guide for the
beginners)

2. Definition
 It is a recording of the electrical activity of the heart from electrodes
placed on the surface of the skin.

3. Normal Physiology Of Dog
Cardiovascular System

4. Electrical Conduction System
Of The Heart
 There is a skeleton of fibrous tissue that
surrounds the conduction system which can
be seen on an ECG.
 Cardiac Myocytes are electrically
excitable.
 Stimulation of a single muscle fibre causes
electrical activity to spread across
myocardium.
 Dysfunction of the conduction system can
cause irregular, fast, or slow heart [cardiac]
rhythms.

5. SA Node :
Generating impulse
from the Right Atrium
and it is the Natural
Pace Maker
generating 60-100bpm
AV node :
Generating impulse from Right
Atria and Right Ventricle.
Gatekeeper Of Heart
generating 40-60bpm
Bundle of hiss :
Backup pacemaker with
intrinsic rate of 40-
60bpm
Left and right bundle
branches :
Backup pacemaker with
intrinsic rate of 20-40bpm
Purkinje fibres :
Backup pacemaker with
intrinsic rate of 20-40bpm

6. Indications of ECG:
 Sinus arrhythmia
 Brachycardiaor tachycardiaor irregularityin the rhythm
 History of syncope or episodic weakness
 Heart diseases
 Cardiac monitoring during anesthesia and criticallyill
patients
 To monitor efficacy of antiarrhythmic therapy
 Systemicdiseases with electrolyte abnormalities
(Hyperkalemia,Hyponatremia, Hypercalcemia,
Hypocalcaemia, Neoplasia , GDV)
 Hypothyroidism and hyperthyroidism

7. Performing An Electrocardiogram
On A Dog
Step 1: Auscultation
 Identification of normal or abnormal heart sounds using
stethoscope or phonendoscope.
 Strongest impulse - systole is felt over the area of the
left apex – 5th Intercostal space
 Heart sounds
 Transient – Short Sounds – LUBB/DUBB
 Murmurs – Occur during silent part of cardiac cycle
 NOTE:
 Quiet room
 Hold mouth shut in Panting dogs

8. Step 2: Proper Patient Positioning
and Restraint
 Right lateral recumbancy on insulatedsurface.
 Don’t let the patient or the clips touch metal.
 Soak the area to be clipped with alcohol.
 Part the fur for good skin contact and attach clips 1"–
2" below elbows and knees.
 Head flat in line with body.
 Legs perpendicular to body (elbows and stiflesare
directly opposite each other).
 Patientmust be still no panting or purring, no
moving.
 Note: Sedation as chemical restraint may alter
the ECG findings.

9. Complications while performing
ECG
ECG without insulated surface
ECG with insulated surface

10. Step 3: Positioning of the leads
 A full set of 8 colouredleads is used
 4 limb leads and 4 chest leads
Limb lead positioning
 Red - right fore leg
 Yellow - left fore leg
 Green - left hind leg
 Black - right hind leg
Chest lead positioning
 Lead VI - right side of thorax at fifth intercostal space
 Lead VII - left side of thorax below sixth intercostal space
 Lead VIII - left side of thorax above sixth intercostal
space

11. Einthoven’s Triangle:
 Einthoven’s Limb Leads :
 Lead I - compares right fore leg with left fore leg
 Lead II - compares right fore leg with left hind leg
 Lead III - compares left fore leg with left hind leg
 Earth - right hind leg

12. Note: A chest lead may be helpful if the P wave is not
clear or if the complexesare small.
Note: A useful site of attachment forthe ECG clips
on the forelimbs is the skin at the flexor angle of the
elbow and for the hind limbs is the skin at the flexor
angle of hock.

13. Holter monitor (24 hrs monitoring device)
• 5 or 7 wire leads, and sticky ECG conductor pads.
Uses :
• Record heart rate variability during normal activity, exercise, and rest or sleep.
• Diagnose the type of arrhythmia in order to determine the correct treatment.
• Determine how well prescribed medications are correcting your pet’s
arrhythmia

14. Step 4: ECG Settings and Recording of Heart
Beat Monitor
 Paper speed :
 The rate of paper (i.e. of recording of the
EKG) is 25 mm/s which resultsin:
 1 mm = 0.04 sec (40 ms) (individual block)
 Calibration:
 voltage can be standardised on paper as
 1 mm = 0.1 mV (individual block)

15. Step 5: Recording the
Electrocardiogram
1. Calculate Rate.
2. Determine Regularity.
3. Assess the P waves.
4. Determine PR interval.
5. Determine QRS
duration.
6. Determine T duration

16. 1. Six strip minute :
 Count the number of RR intervalsbetween 6 seconds in the rhythm strip and multiply by 10 to get
the bpm.
 This method is more effective whenthe rhythm is irregular
 1mm box : .04 sec; 5 small boxes × .o4 = .2o sec
 .20 sec × 5 big boxes = 1 sec
DetermineHEART RATE
3sec 3sec
Interpretation : 9×10 = 90 bpm
1 sec

17. 2. Big box method :
we divide 300 by the no of big boxes between two R’s and is best for regular
rhythm so go by RR or PP interval OR
 Memorize the sequence:
300 - 150 - 100 - 75 - 60 - 50
Interpretation: Approx. 1 box less than 100 = 95 bpm
3
0
0
1
5
0
1
0
0
7
5
6
0
5
0

18. Determine Rhythm And Regularity
 It can be quite variable.It could be:
 Regular : RR intervalconstant
 Regularly irregular :
 RR interval variable but with a pattern.
 Irregularly irregular :
 RR interval variable with no pattern,totally irregular.
Note: In dogs irregularly regular pattern is normal.
Interpretation: Regular

21. ECG Recording Of Electrical
Activity Of The Heart
1. P wave
Atrial depolarisation (systole; contraction)
• Normally present and upright
• If not then indicate arrhythmia
2. QRS wave
Ventricular depolarisation (systole; contraction)
Q wave : It travels in a away from the +ve electrode. Thus
creates a small downward or negative deflection.
R wave : It travels towards the +ve electrode. As it is a large
mass of muscle tissue, it usually creates a large
deflection.
S wave : It travels away from the +ve electrode and is a
small mass of tissue. Thus creates a small negative
deflection .
3. T wave
Ventricular repolarisation (diastole; relaxation)

22. 4. PR interval: Beginning of P wave an beginning of QRS complex
• Abnormality : arrhythmia such as heart blocks
5. QRS interval :
Abnormality : Arrhythmia
Atria Repolarisation?
It is found in QRS because ventricles tend to contraction isstronger than the atria so they mask the
atria repolarisation.

23. Determine P Wave
 Atrial Depolarisation
 Manifested by change in:
 Width :
 Should not exceed .04 sec
 Increase in width: enlargement of left atrium
referred as P mitrale
 Height:
 Should not exceed .4 mV
 Increase in height: enlargement of right atrium
referred to as P pulmonale , resulting from chronic
pulmonary disease.

24.  Absence of p wave:
 Atrial fibrillationor supra ventriculartachycardia
Note:There is no minimum height or width of p wave. Variation of P wave height
is normal finding in dog.
Determine P Wave

25. DeterminePR Interval
 It reflects conduction through AV node
 Normal PR interval is .06 - .13 sec (dogs)
 Short PR interval represents :
 accessory pathwayof conductionwhich allows conductionto by pass AV node
 Prolonged PR interval represents :
 1st degree AV block
Interpretation: 0.12 seconds

26. Determine QRS Interval
 Ventricularenlargement may result in changesin the QRS complex.
 Left ventricularenlargementpattern
 Increased amplitude of the R wave
 Amplitude of R wave greater than 3.0 mV (6 big blocks) (2.5 mV in small-breed dogs)
 QRS duration greater than 0.06 second (large dogs), 0.05 second (small dogs)
 Right ventricularenlargement pattern
 Increasedamplitude of S waves
Interpretation: 0.04 seconds

27. Determine ST Interval
 Elevation of the ST segment
 Greater than 0.15 mV is abnormal in the dog.
 It may be caused by myocardialhypoxia, trans mural myocardial infarction,pericardial
effusion, pericarditis.
 ST segment depression
 Depression of the ST segment greater than 0.2 mV is abnormal in dog.
 It may be caused by myocardial hypoxia, hyperkalemia, hypokalemia, myocardial
infarction, or digoxin toxicity.

28. Determine T wave
 The T wave in dogs and cats is very variable
 It can be negative or positive or even biphasic (i.e. a combination ofboth). This is because
repolarisation of myocardium is very random in animals as comparedto humans.
 So diagnostic value obtainable from the abnormalitiesin the T wave of small animalsis very limited.
 T waves (≤ ¼ of R wave height)
 Tall peaked t waves : Hyperkalemia
 Flattening of t waves : Hypokalemia
Peaked t wave :Hyperkalaemia

29. Electrolyte Abnormalities
 Hypokalemia:
 Moderate: Flattened T wave
 Severe: ST depression
 Hyperkalemia:
 Moderate: Peaked T wave
 Severe: Wide QRS and loss of P wave

30. Variants of T Wave
Inverted T Wave
Hyperacute T Wave

31. Case : Pre and post operative findings
Height of t wave(pre operative) : .8 mV (upright)
(post operative) : .5 mV (inverted)
Height of R wave (pre operative) : 1.5 mV
(post operative) : 1 mV
interpretation : Hyperacute T Wave
Indicative of hyperkalemia/ hypoxia/ myocardial infarction
Pre operative
Post operative

32. Determine QT interval
Normal QT interval : 0.15 to 0.25 second
QT interval : less than half of preceding R-R interval
Interpretation :
• Electrolyteimbalance
• QT interval prolong: Hypokalemia/ hypocalcemia
• Conductiondisturbances
CASE: A 11 year dog operated for pyometra . Findings : R-R interval : 0.28 sec , QT interval : 0.24 sec

33. Arrhythmias
and
Conduction Disturbances

34. Sinus rhythm
 The stimulus originatesfrom the SA node (dominant pacemaker) regularly at a constant
rate, depolarisingthe atria and ventriclesand normally producing a co-ordinated atrio-
ventricularcontraction.This is a normal rhythm.
Case 1: Ca /371 ( Tumorous mass present on the abdominal aspect from
last 3 months no history of heart related problem)
P
QRS
T

35. Sinus Arrhythmia
 The stimulus originatesfrom the SA node but the rate varies (increasesand decreases)
regularly.
 The normal increasein heart rate that occurs
during inspiration.
 In generalsinusarrhythmiascould be:
 Sinus tachycardia
 Sinus bradycardia
Case 2 : animal examined while performing surgery

36. Sinus Tachycardia
 The SA node generatesan impulse and depolarisation at a rate that is faster than normal.
 ECG characteristics
 There is a sinus rhythm but at a faster rate than normal
Case : An adult dog Sinus tachycardia at 210/min ; NORMAL RANGE: Puppy 70-220bpm;
Adult 70-180bpm
Clinicalfindings
The heart rate is faster than normal for age and breed,
with a pulse for every heartbeat (althoughwith faster
rates, the pulse may become weaker).

37. Sinus Bradycardia
 ECG characteristics
 There is a sinus rhythm but at a slower rate than
normal
 Clinical findings
 The heart rate is slower than normal for age and
breed, with a pulse for every heart beat
Case: An adult dog with Sinus bradycardia at 50/min ; NORMAL RANGE: Puppy 70-220bpm;
Adult 70-180bpm
The SA node generatesan impulse and depolarisation at a rate slower than normal . This can
be a normal feature in some giant-breed dogs and in athleticallyfit dogs.

38. Variations In Waves After
AnesthesiaCa/137: animal presented for surgery (aural hematoma with no history of heart related
problems)
1. ECG taken before giving anesthesia HR : 80 bpm
2. ECG taken after 30 minutes during surgery ; after the administration of Atropine
Buturum and Propofol . HR : 150 bpm

39. AV Block
 Conduction abnormalities in the heart where signals are not properly propagated from the
SA node to the AV node into the bundle of hiss and then purkinje system manifested by
Bradycardia, sink in beat and dizziness
 Types of AV BLOCK :
 1st degree AV block: PR interval >200ms with no dropped beats (>5 boxes)
CASE : ECG with prolonged P–R interval of 0.18 to 0.2 s, this is first-degree AV block

40. 2nd degree AV block :
 PR Interval >200ms,(usually there are 3-4 beats and then a beat is dropped because signal is
delayed)
 Second-degree AV Block can be classified :
1. Mobitz type I / Wenckebach’s phenomenon : When P–R interval increases prior
to the block.
2. Mobitz type II : When P–R interval remains constant prior to the block.

41. Rate 50 bpm
Regularity Regularly irregular
P waves Normal, but 4th has no QRS
PR interval lengthens
QRS duration o.o8 sec
Interpretation : 2nd degree AV Block type 1

42. 3rd degree AV block
 When atria and the ventricles contract independently of one another
 Characteristic Findings:
 Constant P-P Intervals and constant Q-Q intervals
 Sometimes P waves could be buried in the QRS complexes
 All conductions through the AV node are blocked and there is no association between
P waves and QRS-T complex. P waves are of normal shape and usually occur at
normal rate .
CASE: ECG with complete third-degree block

43. ATRIAL FLUTTER
 It is used to describe when atria contract at very high rates (greater than 250 beats /min)
giving a flapping or fluttering image to the atria.
 In atrial flutter a re-entrantrhythm is set up in the atria setting up an endless cycle with no
refractory period.
 Atrial flutter is often precursor to atrial fibrillation
Causes:
 Stress
 Ischemia
 Valvular diseases

44.  Observations:
 It is very basic and easy to calibrate
 Heart rate : atria fire at a vey fast rate (>250 bpm)
 P waves: bidirectional saw tooth atrial complexes
 QRS : usually narrow
 Ratio
2:1,3:1,4:1or may vary
 Interpretation:
It indicatesproblem of atrial origin.
Case: Atrial flutter with a 3:1 block

45. Atrial Fibrillation
 One of the most common ,permanent and important arrhythmias seen in small animals.
 Without the presence of the structural heart diseaseor this is referredto as lone AF.

46. Causes:
1. Degenerativevalve disease
2. Dilated cadiaomyopathy
3. Atrial neoplasia
4. Congenitalheart disease
Complication of non cardiac disease:
1. Gastric dilation –volvulusor disordersin
altering vagal tone
2. drug induced (e.g. Digoxin)
CASE: Atrial fibrillation, ECG from a Bull Mastiff with AF with a heart rate of 150/min. This dog
had no underlying heart disease, which is consistent with lone AF.
Observations:
• P waves: There are no consistent and recognisable P
waves
• QRS complexes: Normal and vary in amplitude
• R–R interval: is irregular and chaotic (this is easier to
hear on auscultation)
• Heart rhythm: auscultation sounds are chaotic and
usually quite fast

47. Atrial fibrillation v/s Atrial flutter
 After seeing this video it will be clear why there is no ‘P' wave in ECG in patientswith
Atrial fibrillation.In Atrial fibrillation,atrium doesn't contract it just ripples like
waves....so no 'P' waves. On the other hand in Atrial flutter, atrium contractsbut at a very
fast rate, out of sync with ventricleto produce a seriesof 'P' waves called Flutterwaves.
Flutter / fibrillation ?

49. Murmurs
 They are produced by turbulent blood flow through the
heart and vessels .
 Causes:
 Disruptions of blood flow through valves in the heart
(e.g. ventricular or atrial septal defect),
 Stenotic valve
 An insufficient valve
 Altered blood flow or changes in blood vessel
diameter.
 Murmurs can be evaluated on the basis of their
location and there are four main areas for cardiac
auscultation

51. Valve Point Of Maximum Intensity
Mitral valve Left 5th intercostals space ; Area opposite to the point of the elbow
Aortic valve Left 3 to 4th intercostal space ; Area opposite to Point of the shoulder
Pulmonic valve Left 2 to 3rd intercostal space ; Usually at the axilla
Tricuspid valve Right 3rd to 4th intercostal space

52. Types:
1. Physiologic Murmurs:
 Anaemia , high blood pressure , pregnancy ,athletic
heart.
 They are loudestover Aortic and Pulmonic Areas
2. Innocent Murmurs:
 No known cause and witnessed in young animals
 No louder than grade 3
 Disappear over 5months of age
Ca /290 : animal presented with maggot wound .but was accidently diagnosed
with murmur in the mitral area.
3 Pathologic Murmurs:
Caused by underlying heart
and vessel diseases such as
stenosis of valves, outflow
tract, or great vessels

54. Classification:
Intensity or loudness
 Grade 1: Barely audible
 Grade 2: Audible , but soft
 Grade 3: Easily audible
 Grade 4: Easily audible but with a thrill cannot be palpated on the thorax
 Grade 5: Very loud and a thrill can be palpated on the thorax
 Grade 6: Can be heard without stethoscopeor with stethoscope
Note : Some murmurs can be high or low pitched, harsh blowing or musical.

55. PrematureVentricular Complex
An abnormal beat originatingin the ventriclesand occurring earlier than expectedin relation to
existing rhythm.
Observations :
• No P wave
• QRS wide and bizarre
• T polarityis reversed
• Compensatorypause is longer
R on T Phenomenon : When VPCs occur immediatelyfollowing normal wave within T wave
Case: Snake bite (multiple organ faliure)

56. Causes :
• Structural heart diseases
• Inheritance in GSD
• Hypoxia
• Anemia
• Splenic torsion and pancreatitis
• Use of drugs (anesthesia)
Unifocal VPCs Multifocal VPCs
1. Occurring form one ventricle site. 1. Occurring form more than one ventricle
site.
2. Identical shapes 2. Different shapes
Clinical significance :
• IsolatedVPCs pose insignificant
• Runs of VPCs suggest ventricular tachycardiaand
fibrillation
Case: Swaying gait , exercise intolerance and neurological deficit ; HR: 80 bpm

58. PrematureAtrial Complex
It is the abnormal beat occurring prematurely in the atrial tissue.
Observations :
• Presence of P wave or maybe superimposedon precedingt wave
• QRS normal
• Compensatory pause is shorter

59. Causes :
• Congenital
• Atrial enlargement
• Degenerative valve disease
• Hypoxia
• Chronic obstructive disease
Clinical significance :
• Isolated APCs pose in significance
• Runs of APCs suggest compromised
cardiac output

60. Junctional Premature Complexes
Abnormal beat occurring prematurely and originatingin the AV nodal area.
Observations:
 P wave often inverted
 QRS normal
Causes and clinical significance is similarto APCs

61. Atrial Standstill
 Absence of atrial activity(contractions)due to a failure of atrial muscle depolarisation.
 SA node produce an impulse but the atria are not depolarised.
 Commonly associatedwith hyperkalaemia or atrial cardiomyopathy.
 Continuous absence of P waves but normal heart sounds will be heard (HR: < 60 bpm)
 The impulses are conductedfrom the SA node by internodalpathways to the AV node, which is
termed a sinoventricular rhythm.
 Treatment : Pacemaker implantation
Case: ECG from a Border collie, both with atrial standstill with a nodal escape rhythm at
60/min. Note the absence of P waves. The absence of atrial activity can be confirmed by
echocardiography (25mm/s and 10 mm/mV).

62. INDICATIONS FOR CARDIAC PACING
 Electrical cardiac pacing is most frequently indicated as a treatment PRIMARILY for:
1. Bradyarrhythmias that are accompanied by such clinical signs as syncope, weakness, and
decreased exercise tolerance.
2. Complete atrioventricular (A V) block
3. Permanent atrial standstill
4. Persistent ventricular arrhythmias
Radiograph of implantation-type
pacemaker in place.

63. Pacemaker - Single Chamber -
Atrial
How to interpret presence of pacemaker ?
1. Fusion beats: native beat and pace maker beat
fuse making hybrid QRS complex.
2. Paced spikes
3. Capture beats: native beat breaks through and is
conducted by ventricles.
p

64. Congestive Heart
Failure (CHF)
 It is characterized by high cardiac filling
pressure - venous congestion and tissue fluid
accumulation.
 The location of this fluid is dependent on the
failing ventricle (left-sided,right-sided,or
biventricular failure),and the subsequentsigns
of CHF relate to the magnitude of fluid
accumulation.
 It is a complex clinical syndrome rather than a
specificetiologic diagnosis
 Can be :
1. L-CHF
2. R-CHF

65. L-CHF R-CHF
• Pulmonary hypertension.
• Elevated left atrial pressure.
Etiology: mitral valve insufficiency, mitral
valve stenosis, or systolic or diastolic
dysfunction of the left ventricle.
• In dogs, LCHF causes pulmonary
edema; in cats it may be associated
with either or both pulmonary edema
and pleural effusion.
Clinical signs: tachypnea, respiratory
distress, lethargy, and exercise
intolerance.
Physical examination: Harsh lung
sounds and crackles in patients.
ECG analysis: prolongation of P wave
duration, increased R wave amplitude or
duration, ventricular premature complexes
or tachycardia, or atrial fibrillation.
Emergency therapy: thoracocentesis
• Systemic hypertension.
• elevated right atrial and central venous
pressures (CVPs)
Etiology: tricuspid valve insufficiency or
stenosis, pulmonic valve insufficiency or
stenosis, pulmonary hypertension and
right ventricular systolic or diastolic
dysfunction.
• In dogs, RCHF causes pleural effusion,
ascites, or peripheral edema.
Clinical signs: respiratory distress with
dull
lung sounds. Patients with ascites will
have a
distended abdomen and may have
respiratory
compromise.
Additional indications: presence of
distended jugular veins and prominent
jugular pulses, as well as the presence of
a heart murmur.

66. TREATMENT OF CHF
1. Diuretics – Decrease preload and oedema in dependantparts
• Loop Diuretics
Furosemide – 1 – 2 mg/kg p.o bid to tid
Torsemide – 0.3 mg/kg p.o o.d to bid
• Potassium sparing diuretics
Spirololactone – 1-2mg/kg p.o o.d ,
• Thiazide Diuretics
2. Vasodilator Therapy: reduce preload and afterload. Hydralazine 0.5-2mg/kg PO q12h ;
Amlodipine 0.05 (initial)to 0.3(-0.5) mg/kg PO q12-24h; Prazosin 0.05-0.2mg/kgPO q8-12h
3. Positive Inotropic Agents: are indicatedin managing CHF associatedwith systolic
dysfunctionof the left ventricle. These drugs are administeredin conjunction with diuretic and
vasodilator therapy. Dopamine (dogs and cats, 2 to 10 μg/kg/min CRI); Pimobendan (0.25
to 0.3 mg/kg, PO q12h) has both positive inotropicand vasodilatory effects; Digoxin (0.003 to
0.005 mg/kg PO q12h); Milrinone (dogs, 50 μg/kg slow IV bolus followed by 0.40 to 0.75
μg/kg/minCRI).
4. Oxygen Therapy

67. DILATED CARDIOMYOPATHY
IN DOGS
 Characterized by poor myocardial contractility – with
or without arrhythmias
 Idiopathic in nature
 Large and Giant breedsof dogs most commonly
affected
 Doberman Pinschers, Great Danes, Saint Bernards,
Scottish Deerhounds, Irish
 Wolfhounds, Boxers, Newfoundlands, Afghan Hounds,
and Dalmatians
 Doberman – mutation at 2 chromosomes – 14 (Poor
systolic function) and 5 Ventricular tachycardias)
 Great Danes – X Linked trait

68. PATHOPHYSIOLOGY
• Decreased ventricular contractility – Cardiac remodeling (Chamber dilatation)
• Poor cardiac output – Cardiogenic shock
• Increased cardiac stiffness – increased diastolic pressure – CHF
• Cardiac enlargement – mitral and tricuspid insufficiency
• Reduced perfusion – reduced coronary flow – myocardial infarction

69. CLINICAL SIGNS
• Age – 4 to 10 years
• Males > Females
• Reduced exercise tolerance, syncope
• Auscultation – murmur, gallop sounds and
arrhythmias
• Presenting complaints
• weakness
• lethargy
• tachypnea or dyspnea
• cough (sometimes described as “gagging”)
• anorexia
• abdominal distention (ascites)
• Loss of muscle mass (cardiac cachexia

70. Lateral and dorsoventral views showing
generalized cardiomegaly in a male
Labrador Retriever.

71. Mild mitral regurgitation is
indicated bya relativelysmall area
of disturbed flow in this systolic
frame from a Poodle with dilated
cardiomyopathy.
Note: the LA and LV dilation.
Right parasternallong axis view

72. TREATMENT AND PROGNOSIS
 Congestiveheart failure can be treated with medicationsthat reduce circulatory
congestionand improve heart function.
 Therapy indicatedat betteringquality of life.
 Drugs used:
1. ACE inhibitors
2. Positive inotropic drugs
3. Diuretics
4. Prognosis
Prognosisfor dogs in the occult phase of DCM is guarded, as clinical signs are expected
to develop eventually but this phase may last for months to years.Prognosisfor dogs in the
clinicalphase of DCM is guarded to poor, with survival generally between 5‐8 months
from the time of diagnosis(slightlyless in Doberman Pinschers),but treatment is often
effectiveat alleviating clinicalsigns and improving quality of life.

73. PERICARDIAL EFFUSION
 A pericardialeffusionis excessfluid between the heart and the sac surrounding the
heart known as the pericardium.
 Effusioncan be:
 Haemorrhage – haemangiosarcoma
 Transudate - serosanguinous
 Exudate – Serfibrinous or serosanguinous with high cell count

74. PATHOPHYSIOLOGY
 Fluid accumulation within the pericardial space causes clinical signs when it raises
intrapericardial pressure above normal cardiac filling pressure.
 Impedes venous return and cardiac filling.
 Rapid fluid accumulation or a large effusion causes a steep rise in intrapericardial
pressure, leading to cardiac tamponade

75. CARDIACTAMPONADE
 Cardiac tamponade is a clinicalsyndrome caused by the accumulationof fluid in the
pericardial space resulting in reducedventricularfilling and subsequent hemodynamic
compromise.
 Rate of fluid accumulation is a major contributingfactor to severity of tamponade even
small amounts of rapidly filling fluid can cause sharp rise in intrapericardialpressure.
 The condition is a medical emergency the complications of which include pulmonary
edema, shock, and death.

76. CLINICAL SIGNS
 Clinical findings in patientswith cardiac tamponade usually reflect right-sided CHF and
poor cardiac output.
 Pulsusparadoxus – increasein pulse on inspiration.
 Non specificsigns - lethargy, weakness,poor exercise tolerance,and inappetence.
 Heart sounds are muffled in patients with moderate to large pericardial effusions.

77. Radiograph of a Labrador
with Cardiac Tamponade

78. ECG
• QRS < 1mV
• Electricalalternans may be seen
• ST segment elevation
TREATMENT
• Positive inotropic drugs will be ineffectivein tamponade.
• Pericardiocentesis preferredfirst : 16 to 18 gauge catheterinserted USG guided from underneath
when animal is in right lateralrecumbency – 4th to 6th Intercostalspace.