Download diseases of the cardiovascular system

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•http://www.bostonscientific.com/templatedata/imports/HTML/lifebeatonline/winter2007/l
earning.shtml#fig1
CARDIAC CYCLE
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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
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)
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.
2.5 – 3.5 rib spaces
CANINE WITH CARDIOMEGALY
NORMAL CANINE HEART
Stroke Volume (SV) = EDV – ESV
Cardiac Output (Q) = SV × HR
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.
Failure of pump
• Myocardial dysfunction
– Cardiomyopathy
– Myocarditis
– Taurine deficiency cat
• Circulatory Failure
– Hypovolemia: shock,
hemorrhage, dehydration
– Anemia
– Valvular dysfunction
– Congenital shunts or
defects
DISEASES OF THE
CARDIOVASCULAR SYSTEM:
‘Failure of pump’
Cardiomyopathies
CHF
Valvular disease
Congenital malformation
Infectious
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
CANINE DILATED
CARDIOMYOPATHY
90% of cases occur in Doberman Pinschers and Boxers
OTHER BREEDS INCLUDE WOLFHOUNDS, GREAT DANES, AND COCKER
SPANIELS
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)
The amt. of blood that leaves
The heart
Amt. of blood ejected with
Each cardiac contraction
(affected by afterload, preload,
and inherent contractility)
How often the heart
contracts
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 Reninangiotensin-aldosterone system which leads to
sodium and water retention
THE WALLS OF THE HEART ARE WEAK, FLABBY, AND DILATED – THIS
DILATION MAY CAUSE SEPARATION OF THE MITRAL VALVE LEAFLETS
LEADING TO MITRAL REGURGITATION
CANINE DILATED CARDIOMYOPATHY:
CLINICAL SIGNS
LETHARGY, EXERCISE INTOLERANCE, COUGHING, WEIGHT LOSS, TACHYPNEA,
SYNCOPE, SOFT MURMUR (WHERE?)
CANINE DILATED
CARDIOMYOPATHY:DIAGNOSIS
Enlarged, round heart
DOBERMANS ARE DEEP CHESTED AND MAY NOT APPEAR TO HAVE SUCH AN
ENLARGED HEART ON RADIOGRAPHS
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
CANINE DILATED CARDIOMYOPATHY:
PATHOPHYSIOLOGY, DIAGNOSIS
• Constant stimulation of the heart by the sympathetic
nervous system causes ventricular arrhythmias and
myocyte death
– Most common arrhythmias: VPC’s and ventricular
tachycardia, esp. in boxers & Dobies; other dogs may
have APC’s and atrial fibrillation
ONE VPC
MULTIPLE VPCs
CAUSING TACHY-CARDIA
CANINE DILATED CARDIOMYOPATHY:
DIAGNOSIS: ECHOCARDIOGRAM
http://www.youtube.com/watch?v=7TWu0_Gklzo&feature=related
http://www.youtube.com/watch?v=NSnh3qN2kR4&NR=1
PERFORMING AN ECHOCARDIOGRAM IS THE DEFINITIVE WAY TO DIAGNOSE
DILATED CARDIOMYOPATHY
CANINE DILATED CARDIOMYOPATHY:
TREATMENT
INCREASES CONTRACTILITY
REDUCES FLUID
RETENTION
DIURETIC-ELIMINATES EXCESS
FLUID
CANINE DILATED CARDIOMYOPATHY:
TREATMENT
COENZYME Q10
TAURINE – USED IN COCKER
SPANIELS AND CATS, MAINLY
L-CARNITINE
DIETARY SUPPLEMENTS THAT MAY HELP IMPROVE HEART FUNCTION, ESP
IF THERE IS A DEFICIENCY
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
FELINE DILATED CARDIOMYOPATHY
• In the 1980’s 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
FELINE HYPERTROPHIC
CARDIOMYOPATHY (HCM)
NEUTERED MALE CATS BETWEEN 1-16 YRS. OF AGE
THE MOST COMMON CARDIOMYOPATHY IN CATS!
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
FELINE HYPERTROPHIC
CARDIOMYOPATHY
Blood backs up LA enlarged
FELINE HYPERTROPHIC
CARDIOMYOPATHY: DIAGNOSIS
http://www.youtube.com/watch?v=yNj-lQaUBao
http://www.youtube.com/watch?v=KvUFb4qZwmw&feature=related
http://www.youtube.com/watch?v=xlsq5tJpj04&feature=related
FELINE HYPERTROPHIC
CARDIOMYOPATHY: Pathophysiology
PROBLEM #1: The walls lose compliance and resist filling during
diastole! (diastolic failure)
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”***
FELINE HYPERTROPHIC CARDIOMYOPATHY:
SADDLE THROMBUS
ACUTE, PAINFUL CONDITION CAUSING
PARESIS, COLD REAR LEGS/FEET!
FELINE HYPERTROPHIC CARDIOMYOPATHY:
SADDLE THROMBUS
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
FELINE HYPERTROPHIC
CARDIOMYOPATHY: TREATMENT
FUROSEMIDE (DIURETIC)
ASPIRIN
ANTICOAGULANT
OR
PROPRANOLOL (B-BLOCKER)
Slows HR
Relax so
Time to
fill
DILTIAZEM (CALCIUM CHANNEL BLOCKER)
Inhibits contractility: low BP and cardiac afterload
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
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 >200 beats/min
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
DISEASES OF THE
CARDIOVASCULAR SYSTEM:
Cardiomyopathies
CHF
Valvular disease
Congenital malformation
Infectious
CONGENITAL DEFECTS: PATENT
DUCTUS ARTERIOSUS
CHIHUAHUAS, MALTESE, POODLE, POMERANIAN, SHELTIE
PUPPIES COMMONLY AFFECTED (Table 1-1)
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.
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
CONGENITAL DEFECTS: PATENT
DUCTUS ARTERIOSUS (PDA)
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
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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
PATENT DUCTUS ARTERIOSUS: TREATMENT
EXCELLENT PROGNOSIS WITH SURGICAL CORRECTION: LIGATION OF
THE DUCTUS ARTERIOSUS
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
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 doesn’t, after birth, the blood
will shunt from left to right resulting in overload of the right side of the heart.
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
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.
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
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.
References
• Alleice Summers, Common Diseases of
Companion Animals
• http://veterinarynews.dvm360.com/dvm/article
/articleDetail.jsp?id=156665
• VIN: Robert Prosek DVM, MS, DACVIMCardiology, DECVIM-CA