To understand the heart and mind of a person, look not at what he has already achieved, but at what he aspires to

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To understand the heart and mind of a person,
look not at what he has already achieved, but at
what he aspires to

• -Kahlil Gibran

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VC gt RA gt Triscuspid valve gt RV gt Pulmonary
valve pulmonary a. gt Lungs gt pulmonary v. gt LA gt
Mitral v. gt LV gt Aortic v. gt Aorta gt SYSTEMIC
CIRCULATION gt VC

• http//www.bostonscientific.com/templatedata/impor
  ts/HTML/lifebeatonline/winter2007/learning.shtmlf
  ig1

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(No Transcript)
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CARDIAC CYCLE

• The atria contract in unison and the ventricles
  contract in unison
• The atria and ventricles do not contract at the
  same time (as one group contracts, the other
  relaxes)
• ATRIAL contraction sends blood into the
  ventricles through the bicuspid and tricuspid
  valves
• While this is occurring, the semilunar valves
  close
• The ventricles relax at this time 
• VENTRICULAR contraction sends blood through the
  semilunar valves into the aorta and pulmonary
  artery
• While this is occurring, the bicuspid and
  tricuspid valves close
• The atria relax at this time and blood enters the
  atria from the vena cava and
  pulmonary veins
• SYSTOLE contraction of the atria and ventricles
  
• blood is being ejected from the heart
• DIASTOLE relaxation of the atria and ventricles
  -heart is filling with blood

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HEARTBEAT Lub-dub S1 and S2

• S1 Beginning of systole (pulse)
• increase in intraventricular pressure during
  contraction exceeds the pressure within the atria
• closing AV valves (mitral first)
• contraction forces blood semilunar valves.

• S2 Beginning of Diastole (no pulse)
• ventricles begin to relax
• pressures within the heart become less than the
  semilunar valves,
• causes the semilunar valves to snap shut (aortic
  first)

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STROKE VOLUME

• Contractility  Contractility is the intrinsic
  ability of cardiac muscle to develop force for a
  given muscle length.  It is also referred to as
  inotropism.
• Preload  Preload is the muscle length prior to
  contractility, and it is dependent of ventricular
  filling (or end diastolic volume.)  This value is
  related to right atrial pressure.  The most
  important determining factor for preload is
  venous return.
• Afterload  Afterload is the tension (or the
  arterial pressure) against which the ventricle
  must contract.  If arterial pressure increases,
  afterload also increases. Afterload for the left
  ventricle is determined by aortic pressure,
  afterload for the right ventricle is determined
  by pulmonary artery pressure.      

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2.5 3.5 rib spaces
CANINE WITH CARDIOMEGALY
NORMAL CANINE HEART
Stroke Volume (SV) EDV ESV Cardiac Output (Q)
SV HR
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MURMURS

• I - Lowest intensity, difficult to hear even by
  expert listeners
• II- Low intensity, but usually audible by all
  listeners
• III - Medium intensity, easy to hear even by
  inexperienced listeners, but without a palpable
  thrill
• IV - Medium intensity with a palpable thrill
• V - Loud intensity with a palpable thrill.
  Audible even with the stethoscope placed on the
  chest with the edge of the diaphragm
• VI - Loudest intensity with a palpable thrill.
  Audible even with the stethoscope raised above
  the chest.

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Failure of pump

• Myocardial dysfunction
• Cardiomyopathy
• Myocarditis
• Taurine deficiency cat

• Circulatory Failure
• Hypovolemia shock, hemorrhage, dehydration
• Anemia
• Valvular dysfunction
• Congenital shunts or defects

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DISEASES OF THE CARDIOVASCULAR SYSTEM Failure
of pump

• Cardiomyopathies
• CHF
• Valvular disease
• Congenital malformation
• Infectious

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DX Heart Disease

• HISTORY cats usually acute
• PHYSICAL EXAMINATION cyanosis R to L shunt
• ANCILLARY TESTS- electrocardiography-
  radiography- echocardiography (including Doppler
  Echocardiography)- cardiac catheterization
• RESPONSE TO THERAPY

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CANINE DILATED CARDIOMYOPATHY
90 of cases occur in Doberman Pinschers and
Boxers
OTHER BREEDS INCLUDE WOLFHOUNDS, GREAT DANES, AND
COCKER SPANIELS
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CANINE DILATED CARDIOMYOPATHY PATHOPHYSIOLOGY

• DECREASED CONTRACTILITY FROM AN UNKNOWN CAUSE
  (viral?, carnitine deficiency?)
• Decreased contractility decreased cardiac output

CO (CARDIAC OUTPUT) SV (STROKE VOLUME) X HR
(HEART RATE)
Amt. of blood ejected with Each cardiac
contraction (affected by afterload, preload, and
inherent contractility)
How often the heart contracts
The amt. of blood that leaves The heart
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CANINE DILATED CARDIOMYOPATHY PATHOPHYSIOLOGY

• THE BODY COMPENSATES BY
• 1. INCREASING THE HEART RATE
• this is done by sympathetic nervous system
  stimulation
• 2. TRYING TO INCREASE STROKE VOLUME BY
  INCREASING PRELOAD (this means that the body
  increases filling of the heart)
• This is done by activation of the
  Renin-angiotensin-aldosterone system which leads
  to sodium and water retention

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THE WALLS OF THE HEART ARE WEAK, FLABBY, AND
DILATED THIS DILATION MAY CAUSE SEPARATION OF
THE MITRAL VALVE LEAFLETS LEADING TO MITRAL
REGURGITATION
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CANINE DILATED CARDIOMYOPATHY CLINICAL SIGNS
LETHARGY, EXERCISE INTOLERANCE, COUGHING, WEIGHT
LOSS, TACHYPNEA, SYNCOPE, SOFT MURMUR (WHERE?)
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CANINE DILATED CARDIOMYOPATHYDIAGNOSIS
Enlarged, round heart
DOBERMANS ARE DEEP CHESTED AND MAY NOT APPEAR TO
HAVE SUCH AN ENLARGED HEART ON RADIOGRAPHS
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CANINE DILATED CARDIOMYOPATHY DIAGNOSIS
PULMONARY EDEMA OCCURS IN LEFT-SIDED HEART FAILURE
PLEURAL EFFUSION OCCURS IN RIGHT SIDED HEART
FAILURE
PATIENT MAY SHOW SIGNS OF LEFT-SIDED,
RIGHT-SIDED, OR HEART FAILURE FROM BOTH SIDES
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CANINE DILATED CARDIOMYOPATHY PATHOPHYSIOLOGY,
DIAGNOSIS

• Constant stimulation of the heart by the
  sympathetic nervous system causes ventricular
  arrhythmias and myocyte death
• Most common arrhythmias VPCs and ventricular
  tachycardia, esp. in boxers Dobies other dogs
  may have APCs and atrial fibrillation

ONE VPC
MULTIPLE VPCs CAUSING TACHY-CARDIA
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CANINE DILATED CARDIOMYOPATHY DIAGNOSIS
ECHOCARDIOGRAM
http//www.youtube.com/watch?v7TWu0_Gklzofeature
related
http//www.youtube.com/watch?vNSnh3qN2kR4NR1
PERFORMING AN ECHOCARDIOGRAM IS THE DEFINITIVE
WAY TO DIAGNOSE DILATED CARDIOMYOPATHY
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CANINE DILATED CARDIOMYOPATHY TREATMENT
INCREASES CONTRACTILITY
REDUCES FLUID RETENTION
DIURETIC-ELIMINATES EXCESS FLUID
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CANINE DILATED CARDIOMYOPATHY TREATMENT
TAURINE USED IN COCKER SPANIELS AND CATS, MAINLY
L-CARNITINE
COENZYME Q10
DIETARY SUPPLEMENTS THAT MAY HELP IMPROVE HEART
FUNCTION, ESP IF THERE IS A DEFICIENCY
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FELINE DILATED CARDIOMYOPATHY
A globular-shaped heart with severe dilation of
all four chambers. Depressed ventricular
contractile performance occurs. Ventricular
dilation distorts the atrioventricular valves
leading to mitral regurgitation and
atrial enlargement
ABNORMALLY THIN VENTRICULAR WALLS
ATROPHIED PAPILLARY MUSCLES
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FELINE DILATED CARDIOMYOPATHY

• In the 1980s DCM in cats was one of the most
  commonly diagnosed heart diseases. It was
  discovered that this was caused by a deficiency
  of TAURINE, an amino acid.
• Since that time commercial foods have added
  taurine to feline diets, which has significantly
  decreased the number of cases of feline DCM

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FELINE HYPERTROPHIC CARDIOMYOPATHY (HCM)
NEUTERED MALE CATS BETWEEN 1-16 YRS. OF AGE
THE MOST COMMON CARDIOMYOPATHY IN CATS!
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FELINE HYPERTROPHIC CARDIOMYOPATHY

• THE PREDOMINANT PATHOLOGY OF THIS DISEASE IS LEFT
  VENTRICULAR HYPERTROPHY
• CAUSE
• /- genetics
• related to abnormal myocardial myosin or calcium
  transport within the muscles of the heart

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FELINE HYPERTROPHIC CARDIOMYOPATHY
Blood backs up LA enlarged
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FELINE HYPERTROPHIC CARDIOMYOPATHY DIAGNOSIS
http//www.youtube.com/watch?vyNj-lQaUBao
http//www.youtube.com/watch?vKvUFb4qZwmwfeature
related
http//www.youtube.com/watch?vxlsq5tJpj04feature
related
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FELINE HYPERTROPHIC CARDIOMYOPATHY
Pathophysiology
PROBLEM 1 The walls lose compliance and resist
filling during diastole! (diastolic failure)
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FELINE HYPERTROPHIC CARDIOMYOPATHY
Pathophysiology

• PROBLEM 2 If the left ventricle cannot fill
  adequately with blood, the blood backs up into
  the left atrium (enlargement) ? pulmonary veins ?
  pulmonary edema!
• PROBLEM 3 The left atrium becomes dilated with
  blood ? the blood becomes static ? blood stasis
  leads to clot formation ? clot becomes dislodged
  and trapped elsewhere in the arterial system ?
  thromboembolism!

90 of thrombi become lodged in the aortic
trifurcation causing saddle thrombus
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FELINE HYPERTROPHIC CARDIOMYOPATHY SADDLE
THROMBUS
ACUTE, PAINFUL CONDITION CAUSING PARESIS, COLD
REAR LEGS/FEET!
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FELINE HYPERTROPHIC CARDIOMYOPATHY SADDLE
THROMBUS
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FELINE HYPERTROPHIC CARDIOMYOPATHY CLINICAL
SIGNS and DIAGNOSIS

• Soft, sytolic murmur (grade 2-3/6)
• Gallop rhythms or other arrhythmias
• ECG ? p wave duration, ? QRS width, sinus
  tachycardia
• Echo shows ? ventricular wall thickness, dilated
  left atrium
• Acute onset of heart failure
• Acute onset of systemic thromboembolism
• Hindlimb paresis
• Cold rear legs
• Painful rear legs

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FELINE HYPERTROPHIC CARDIOMYOPATHY TREATMENT
FUROSEMIDE (DIURETIC)
ASPIRIN
ANTICOAGULANT
Relax so Time to fill
OR
DILTIAZEM (CALCIUM CHANNEL BLOCKER) Inhibits
contractility low BP and cardiac afterload
PROPRANOLOL (B-BLOCKER) Slows HR
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FELINE HYPERTROPHIC CARDIOMYOPATHY TREATEMENT

• LASIX (furosemide) a diuretic used to treat
  pulmonary edema
• DILTIAZEM a calcium channel blocker used to
  inhibit cardiac and vascular smooth muscle
  contractility reduces blood pressure and cardiac
  afterload overall improvement in diastolic
  function
• Or Propranolol a beta-blocker to decrease heart
  rate and myocardial oxygen demand
• ASPIRIN an anticoagulant used to thin blood and
  help prevent clot formation in HCM
• TPA (Activase) serves as a fibrolysin resulting
  in the breakdown of clots that have already
  formed
• Or Heparin, Warfarin acts on the coagulation
  factors to inhibit the formation of a stable clot

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FELINE HYPERTROPHIC CARDIOMYOPATHY CLIENT INFO

• There is no cure!
• Cats with HCM may experience heart failure,
  arterial embolism, or SUDDEN DEATH!
• Cats whose heart rates stay below 200 beats/min
  have a better prognosis than those whose heart
  rate is gt200 beats/min

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CANINE HYPERTROPHIC CARDIOMYOPATHY

• An UNCOMMON canine disease, but the cause
  appears to be heritable
• CLINICAL SIGNS
• Fatigue
• Sudden death
• Tachypnea
• Syncope
• Cough
• BREEDS German Shepherds, Rottweilers, Cocker
  Spaniels, and others

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DISEASES OF THE CARDIOVASCULAR SYSTEM

• Cardiomyopathies
• CHF
• Valvular disease
• Congenital malformation
• Infectious

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CONGENITAL DEFECTS PATENT DUCTUS ARTERIOSUS
CHIHUAHUAS, MALTESE, POODLE, POMERANIAN, SHELTIE
PUPPIES COMMONLY AFFECTED (Table 1-1)
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CONGENITAL DEFECTS PATENT DUCTUS ARTERIOSUS
Normally, the ductus arteriosus carries blood
from the pulmonary artery to the aorta during
fetal development. It bypasses the lungs of the
fetus.
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CONGENITAL DEFECTS PATENT DUCTUS ARTERIOSUS
The duct should close in the first 12-24 hours
after birth. If it does not, the blood begins to
shunt from the aorta into the pulmonary artery
and hyperperfuse the lungs. The left side of the
heart will have an increase in blood return and
become volume overloaded. Left heart failure
THIS IS CALLED A LEFT-TO-RIGHT SHUNT
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CONGENITAL DEFECTS PATENT DUCTUS ARTERIOSUS (PDA)
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CONGENITAL DEFECTS PATENT DUCTUS ARTERIOSUS

• CLINICAL SIGNS
• A loud murmur best heard over the left base
• Sometimes called a machinery murmur or a
  continuous murmur (btw S1 and S2)
• If the shunt is small some animals may be
  asymptomatic
• In large shunts the animal will develop
  left-sided heart failure
• Pulmonary edema
• Cough
• Exercise intolerance
• Tachypnea
• Weight loss
• ECG wide range of arrhythmias including APCs and
  VPCs
• Echocardiography (ultrasound)
• Radiographs left atrial and ventricular
  enlargement

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PATENT DUCTUS ARTERIOSUS TREATMENT
EXCELLENT PROGNOSIS WITH SURGICAL CORRECTION
LIGATION OF THE DUCTUS ARTERIOSUS
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PATENT DUCTUS ARTERIOSUS TREATMENT

• CLIENT INFO
• 64 OF ANIMALS WILL DIE WITHIN 1 YEAR IF NOT
  TREATED SURGICALLY
• Dogs with this condition should not be used for
  breeding

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ATRIAL AND VENTRICULAR SEPTAL DEFECTS Cats
Atrial Septal Defect
During fetal life, the foramen ovale is an
openingi n the interatrial septum, allowing
shunting of blood from the right atrium to the
left atrium in order to bypass the nonfunctioning
fetal lungs. It should close at birth. If it
doesnt, after birth, the blood will shunt from
left to right resulting in overload of the right
side of the heart.
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CONGENITAL DEFECTS ATRIAL AND VENTRICULAR SEPTAL
DEFECTS

• CLINICAL SIGNS ATRIAL SEPTAL DEFECTS
• Result in overload of the right side of the heart
  ? dilation and hypertrophy of the right-sided
  chambers
• Systolic murmur
• Right-sided heart failure
• Radiographs right ventricular enlargement
• Echo right ventricular dilatation

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CONGENITAL DEFECTS ATRIAL AND VENTRICULAR SEPTAL
DEFECTS
Blood is shunted from the oxygen-rich left
ventricle into the right ventricle. The blood
goes through pulmonary circulation and right
back into the left atrium and ventricle resulting
in volume overload of the left side of the heart
(LHF). The right ventricle may dilate as well.
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CONGENITAL DEFECTS ATRIAL AND VENTRICULAR SEPTAL
DEFECTS

• CLINICAL SIGNS VENTRICULAR SEPTAL DEFECTS
• Animals with small defects may have minimal or no
  signs
• Larger defects may result in acute left-sided
  heart failure, usually by 8 weeks of age
• A harsh holosystolic murmur
• CLIENT INFO
• Repair of these defects requires open-heart
  surgery or cardiopulmonary bypass. These
  procedures are uncommon in the dog and cat
• Most of these animals will eventually experience
  development of congestive heart failure

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VSD - Treatment

• There are 2 current surgical options available. 
• Before right-to-left shunting has developed,
  pulmonary artery banding
• decrease the blood flow across the defect
• reducing the overload on the lungs and the left
  heart. 
• Repair of the defect, but this requires open
  heart surgery and carries a high risk.

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References

• Alleice Summers, Common Diseases of Companion
  Animals
• http//veterinarynews.dvm360.com/dvm/article/artic
  leDetail.jsp?id156665
• VIN Robert Prosek DVM, MS, DACVIM-Cardiology,
  DECVIM-CA