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290 Cards in this Set
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in regards to signalment: what type of diseases/conditions do young animals have compared to old animals when dealing with the CV system |
young: congenital lesions such as aortic stenosis |
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what breed are more susceptible to getting DCM
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Dobermans
Irish wolfhounds Great danes |
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What breed is especially susceptible to getting endocardiosis
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calvalier king charles spaniels
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what is a common presenting complaint of dogs with left sided CHF
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a chronic productive cough
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why does dyspnea occur with left CHF
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it occurs as pulmonary edema and/or pleural effusion increases the effort required for respiration.
may see air hunger position in severe cases |
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besides pulmonary edema or pleural effusion what else can dyspnea result from
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diaphragmatic hernias
fractured ribs tracheal foreign bodies/neoplasms pneumonia/pulmonary neoplasia |
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T/F: ascites is the result of left sided CHF
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False: right sided CHF; may also be the result of liver disease, hypoalbuminemia, etc
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what are the major steps in the examination of the heart and circulatory system
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temperature
pulse respiration mucous membranes thoracic palpation ausculation heart percussion abdominal palpation observation or peripheral blood vessels |
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what is the temperature like in animals with heart failure
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usually normal or subnormal
may be elevated with myocarditis, valvular endocarditis, hyperthyroidism |
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which three characteristics of the pulse are considered in a physical exam
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pulse rate, rhythm, and quality
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what can an increased pulse rate be due to?
what about a decreased pulse rate? |
increased: tachycardia (may occur with heart failure), fear and excitement, pain and elevated temperature
decreased: bradycardia (occurs during sleep), excessive parasympathetic tone and disease of the conduction system of the heart |
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what must the pulse rate always be compared to and why
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the auscultated heart rate to detect pulse deficits
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when dealing with the pulse, what can indicate an arrhythmia is present
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variable time intervals between pulses
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what is regular-respiratory sinus arrhythmia
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the pulse rate increases as the dog inspires and decreases with exhalation as a result of changes in venous return and vagal tone during respiration.
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relates to the amplitude and duration of the pulses
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pulse quality
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what are some abnormalities of pulse quality
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large strong (hyperkinetic) pulses |
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a marked difference in pressure from pulse to pulse
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alternating pulses
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what is an example of alternating pulses
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atrial fibrillation
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the artery is abnormally distended by each pulse with is larger than normal
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large strong (hyperkinetic) pulses
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example of hyperkinetic pulse
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exercise
anemia |
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strong pulse with a sharp rise and fall in pulse pressure. associated with a marked variation between systolic and diastolic pressure
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waterhammer pulses
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give an example of waterhammer pulses
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arterio-venous shunts
severe anemia |
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the pulses are weak and of short duration
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small weak (hypokinetic) pulses
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examples of hypokinetic pulses
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DCM |
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what information do the mucous membranes provide on the CV system
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info on perfusion
pale color = severe left heart failure; cardiogenic shock cyanotic = right to left shunts; severe left heart failure brick red = erythrocytosis or R-L shunts delayed CRT = decreased ventricular ooutput or peripheral VC |
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what is auscultated at the site of the apical beat
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the mitral valve (5th-6th intercostal space on the left in the middle of the vental third of the thorax in the dog)
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what can shift the apical beat cranially
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tumors, abscesses or hernia in the caudal thorax
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what can shift the apical beat caudally
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cranial thoracic tumor or abscesses and cardiac enlargement
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what makes the apical beat stronger
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young animal
thin animals anemia pyrexia excitement fear pain hyperthyroidism shunts cardiac enlargement |
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what makes the apical beat weaker
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shock |
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T/F: both sides of the chest should be auscultated
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true
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what are the normal heart sounds
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there are four but only two are audible in dogs and cats
S1 = closure of the AV valves, this is lub; can be heard just before pulse is palpated S2 = softer, of shorted duration and higher in pitch than S1 (this is dub) S3 = occurs as a result of rapid passive ventricular filling S4 = occurs as a result of contraction of the atria |
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which heart sounds are normally heard in the dog and cat
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S1 and S2 |
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where is S2 best heard
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over the aortic and pulmonary valves (4th left intercostal space at the point of the shoulder, 3rd left intercostal space midway b/w point of shoulder and sternum)
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what does the S3 sound usually occur with
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massive left ventricular displacement
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when might S4 be heard
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when there is reduced ventricular compliance--HCM in cats,, ventricular hypertrophy secondary to aortic stenosis in dogs
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what is a gallop rhythm and how is it classified
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the presence of an extra heart sound |
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what are murmurs
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audible vibrations produced by turbulent blood blow through an area.
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what are some causes of murmurs
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narrowing of a vessel (pulmonic or aortic)
valvular insufficiency (endocardiosis, idiopathic DCM, valvular endocarditis) increased rate of blood flow (anemia, fever, shunts, etc) decreases in viscosity of the blood |
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what criteria should a murmur follow for classification
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physiological or pathological
when occurs in cardiac cycle location and radiation of murmur intensity or loudness of murmer |
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classification of intensity of murmurs
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1 = very soft, occurs only over small area and is heard after prolonged auscultation |
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T/F: heart percussion is of little value in dogs and cats
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true
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when might distension of the jugular vein be present
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right CHF
pericardial effusion |
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what are the special diagnostic tests available for the CV system
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radiography
ECG echocardiography cardiac catheterization phonocardiogram |
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what view/position should never be used for a radiograph in an animal with respiratory distress or pleural/pericardial effusions
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VD
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what are radiographs useful for when evaluating the CV system
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abnormalities in the blood vessels, airways, lung parenchyma, and pleural space
can reveal changes in heart size |
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what is the main use of an ECG
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to characterize arrhythmias and conduction disturbances.
can provide information of the size of the heart chambers, myocardial hypoxia and electrolyte imbalances |
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what is echocardiography useful for
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providing information on size and motion of the heart chambers
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what can cardiac catheterization tell you
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can measure pressures and oxygen saturation levels in the hear the camber; determine blood flow; biopsies can be taken
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what is a phonocardiogram and what info can it tell you
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a graphic representation of the heart sounds on an ECG tracing.
can differentiate gallop rhythms |
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what is the ECG mainly used for and what info can it give us
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to determine heart rate and conduction disturbances. |
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technique for recording an ECG (include the process)
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place animal in RLAT on rubber mat. extend limbs perpendicular to long axis of body and attach leads to elbows and cranial aspects of stifles. alcohol/ECG gel is used to facilitate conduction from skin to electrodes. a rhythm strip is recorded using lead 2 and paper speed of 50mm/sec
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how many heart beats are recorded for each lead
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about 5 at a paper speed of 25mm/sec and sensitivty of 1cm = 1mV
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how many heart beats are on the rhythm strip
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15-20
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T/F: animals in respiratory distress can have a rhythm strip taken with the animal in any position that is comfortable to the patient for determining arrhythmias
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true
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steps for examining an ECG
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ensure it is free of artifacts
use paper speed to determine rates find mean electrical axis assess atrial size assess ventricular size assess the ST segment assess QT interval assess T wave determine is arrhythmia is present |
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normal heart rate for:
dogs toy breeds puppies cats |
70-160
<180 <220 120-240 |
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what is the mean electrical axis (MEA)
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the average direction in which depolarization spreads through the ventricular myocardium in systole
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normal MEA for the dog
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+40 to +100 degrees
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normal MEA for the cat
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0 to +160 degrees
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what does a greater than normal MEA indicate
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right ventricular enlargement or right bundle branch block
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what does a smaller than normal MEA indicate
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left ventricular enlargement or left bundle branch block
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left atrial enlargement if P wave is too wide in lead two = P mitrale: what are values in dogs and cat
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dog = >.04 second
LBD >.045 seconds cat > .04 seconds |
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right atrial enlargement if P wave is too high in lead two = P pulmonale: what are values for dog and cat
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Dog >.4 mV
cats: >.2 mV |
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biatrial enlargement is
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if P wave is too tall and too wide in lead two
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indications of left ventricular enlargement in dogs
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increased voltage R waves in lead 2:
small dog (<20kg): R >2.5mV large dog: R >3.0 mV duration of QRS increased in lead 2: small dog: QRS >.05seconds large dog: QRS>.06seconds giant breeds: QRS >.065seconds |
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indications of left ventricular enlargement in cats
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increased voltage of the R wave in lead 2 (>,9mV) is the only indicator of left ventricular enlargement
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indications of right ventricular enlargement in dogs
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S wave seen in leads 1, 3, and aVF
increased MEA |
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indications of right ventricular enlargement in cats
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increased MEA
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why are you not able to detect biventricular enlargement on an ECG
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becasue of the greater muscle mass and hence influences of the left ventricule on teh ECG
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a delay in conduction in the right bundle branch result in delyaed activation of the right ventricle --> the QRS complex to widen with large wide S waves in leads 1, 2, 3, and aVF
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right bundle branch block
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what can cause right bundle branch block
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infection, neoplasia, infarction, fibrosis, or cardiac trauma.
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DDX for right bundle branch block
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right ventricular enlargement, ventricular premature depolarizations
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the conduction delay of _____________ means the left ventricule is activated later than normal and the QRS complexes in leads 1, 2, 3, and aVF are prolonged. also may progress to complete heart block or more serious arrhythmias
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left bundle brach block
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DDX for left bundle branch block
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left ventricular enlargement
VPC |
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what can low voltage QRS complexes indicate
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may indicate obesity, pleural or pericardial effusion, hypothyroidism, pneumothorax, or diffuse myocardial disease
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when assessing the ST interval, what does depression from baseline or elevation indicate
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myocardial ischemia
other signsL wide QRS/bizzare QRS tall T waves notched R wave |
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normal QT levels for the dog and cat
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dog = .15 to .25 seconds
cat = .12 to.18 seconds they are inversely proportional to the heart |
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what does the T wave look like when there is hyperkalemia
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tall and spiked
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what is an arrhythmia
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an abnormality in the rate, rhythm or flow of depolarization through the heart
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a complex neuroendocrine syndrome in which endogenous compensatory mechanisms that provide effective short term circulatory support contribute to progressive cardiac dysfunction and death
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heart failure
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what is heart failure the end result of
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most heart disease
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when does heart failure occur
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when CO is insufficient to meet the needs of the tissues
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what are some examples of heart disease
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murmurs
arrhythmias other cardiac abnormalities |
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when are signs of heart failure generally seen
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when heart disease is severe
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how is CO restored in the short term
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the SNS gets activated and causes increased contractility and heart rate along with VC of the arteries and veins
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how is CO restored when there is hemorrhage for example
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other compensatory mechanisms come into play. decreased renal blood flow causes the RAAS to be activated which results in peripheral VC and Na and water retention by the kidneys.
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T/F: the higher the NE levels that shorter the survival time of a dog in heart failure
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true
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what does chronic VC due to RAAS result in
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increased afterload and MVO2 of the heart and decreased forward flow and predisposes to hypotension
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causes increased sympathetic activity and causes hypertrophy and remodeling of the ventricle
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ANG2
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causes vascular and myocardial fibrosis, direct vascular damage and baroreceptor dysfunction, and potentiates the effects of NE
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aldosterone
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what does stimulation of RAAS and increased ACE result in
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increased breakdown of bradykinin which normally causes VD trhough NO and prostacyclin activation
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occurs in heart disease and is a response to chronically increased tension on myocardial fibers and ANG2
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cardiac hypertrophy
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causes by chronic increased diastolic pressure (volume overload)
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eccentric hypertrophy
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what is eccentric hypertrophy characterized by
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by cells elongating by the additioon of sarcomeres in series (end to end) which results in a larger ventricle with an increased chamber size but with walls of normal thickness
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occurs when there is increased systolic ventricular pressure (pressure overload)
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concentric hypertrophy
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what is concentric hypertrophy characterized by
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the sarcomeres replicate side by side/in parallel resulting in wider cells and a thicker/less distensible ventricular wall which is less able to dilate in diastole (lysotrophy)
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T/F: hypoxia decreases the efficiency of the heart muscle contraction and promotes arrhythmias
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true
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what are the signs of left sided CHF
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hypotension, pale MM,, prolonged CRT, tachycardia, weak pulses, lethargy, depression, weakness, exercise intolerance, pre-renal azotemia. may see pulmonary edema, coughing, dyspnea, orthopnea, tachypnea, cyanosis
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signs of right sided CHF
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distension of jugular vein, ascites, hepato and splenomegaly, pleural effusion, and rarely peripheral edema. due to the decreased venous return to the left ventricle may see hypotension, lethargy, depression, weakness, etc
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phases of CHF
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1= heart disease and no signs
2= cough, fatigue and dyspnea with normal or strenuous exercise 3= cough, fatigue, dyspnea, orthopnea at night or with any activity 4= cough, fatigue, dyspnea, orthopnea, and cyanosis at rest |
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what are the general principles of heart failure treatment
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handle animals with extreme care
drugs: morphine (nausea and vomiting no desirable though), diazepam, butorphanol enhance oxygenation: drain fluid, O2 reduce edema using diuretics further reduce preload--NG for example ACE inhibitors improve contractility IV fluids are given with caution treatarrhythmias low Na diet beta blockers frequent PE |
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in heart failure when is supplemental O2 indicated and what is the goal of O2 therapy
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severe HF with dyspnea
goal is to maintain PaO2 >60mmHg |
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what percentage O2 is usually given to HF patients and why
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35-50% b/c 100% for long periods can be toxic to the respiratory epithelium, also the O2 contains no moisture so it dries the respiratory mucosa
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ways to deliver O2
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face mask
O2 collars nasal catheters transtracheal catheters O2 cages ventilation support |
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what is the most commonly used diuretic for reducing edema by decreasing circulating blood volume
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furosemide
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what is the most important drug used in the treatment of CHF
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furosemide
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once a CHF patient is stable what is another diuretic that can be used
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spironolactone
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furosemide may be a life saver but it does have some undesirable effects. what are some of them
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activates RAAS and may cause decreases CO and hypotension, dehydration, azotemia, and electrolyte disturbances
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what do ACE inhibitors do (benefits)
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slow progression of HF
blunten pathological remodeling and fibrosis due to ANG2 and aldosterone, enable up to 50% reduction in furosemide dosage, prolong and improve quality of life |
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what are the most widely used vasodilators in the therapy of CHF
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ACE inhibitors
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phosphodiesterase inhibitor that causes arterio and venodilation
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Pimobendan
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what drug can be used as a CRI if an animal is in cardiogenic shock
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dobutamine
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what do loading doses of digoxin usually result in
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toxicity
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commonly used Beta blockers in CHF
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metoprolol
carvedilol |
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downfall to using beta blockers
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cosr
negative inotropic effects |
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what does the following indicate: progressive reudction in serum Na levels, progressive heart enlargement, and progressive reductions in echo indices
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progression of heart failure
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when do congenital heart disease begin and what are they due to
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begin during fetal development and are due to inherited defects, genetic mutations or a developmental accident that is not coded genetically
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T/F: congenital heart disease is seen more in cats than dogs
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false--seen more in dogs
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what are the most common congenital disorders in the dog
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PDA
aortic stenosis VSD pulmonic stenosis ASD |
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what are the most common congenital abnormalities in the cat
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AV valve malformation
VSD aortic stenosis endocardial fibroelastosis PDA tetralogy of fallot |
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describe fetal circulation
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Blood from the placenta is carried to the fetus by the umbilical vein. About half of this enters the fetal ductus venosus and is carried to the inferior vena cava, while the other half enters the liver proper from the inferior border of the liver. . The blood then moves to the right atrium of the heart. In the fetus, there is an opening between the right and left atrium (the foramen ovale), and most of the blood flows through this hole directly into the left atrium from the right atrium, thus bypassing pulmonary circulation. The continuation of this blood flow is into the left ventricle, and from there it is pumped through the aorta into the body.
Some of the blood entering the right atrium does not pass directly to the left atrium through the foramen ovale, but enters the right ventricle and is pumped into the pulmonary artery. In the fetus, there is a special connection between the pulmonary artery and the aorta, called the ductus arteriosus, which directs most of this blood away from the lungs |
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what is the ductus arteriosus
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a vessel that connects the aorta to the PA in the fetus. normally this vessel closes after birth and becomes the ligamentum arteriosum
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pathophysiology of PDA
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duct remains patent to a greater or lesser degree after birth. Blood is shunted from left to right (aorta to PA) b/c of lower pressure in the pulmonary system. as a result of this shunting volume overload occurs and eccentric hypertrophy and left sided CHF can occur. in patients with large PDAs over circulation can occur and an increase in pulmonary pressure can shift the flow to right to left which can lead to right sided hypertrophy and heart failure. if flow changes to right to left there will be low PaO2 going to the body and the kidneys will release EPO and thus increases in blood viscosity can occur
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signalment for PDA
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seen most commonly in toy and mini poodles and GSD
more common in females detected at first vaccination in poodles it is transmitted as a polygenic trait |
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T/F: most animals that have a PDA are asymptomatic and thus this is an incidental finding at first vaccination
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true
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when are signs of heart failure usually seen in dogs with a PDA
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by 16 months
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T/F: signs of a PDA relate to the degree of shunting and the direction
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true
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what is the hallmark PE finding of a PDA
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a continuous "machinery" murmur that is loudest forward of the heart base. this murmur is audible throughout systole, when it is loudest, and is present in most of diastole
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what other signs are seen in a PDA patient besides the characteristic murmur
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a precordial thrill
bounding or water hammer femoral pulses with right to left shunts cyanosis occurs caudally |
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PDA findings in radiographs
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signs of left heart enlargement and failure may be present with left to right shunts
signs of right heart enlargement with right to left shunts sometimes can see PDA |
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what are some diagnostics that you can perform in patients with a PDA
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imaging
echo doppler angiopathy ECK |
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treatment of PDA
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no drugs will close it
surgical correction in left to right shunts correct as soon as possible, if in heart failure stabilize the patient first cannot surgically fix right to left PDAs |
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DDX for PDA
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concurrent aortic stenosis and aortic insufficiency
pulmonic stenosis with pulmonic regurgitation VSD with aortic regurgitation aorticopulmonary window truncus arteriosis |
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how do you prevent PDA
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do not breed the dog
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T/F: aortic stenosis is not common in cats
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true
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pathophysiology of aortic stenosis
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the stenosis causes increased afterload resulting in left ventricular concentric hypertrophy and as a result there is less diastolic filling and less CO.
ventricles are predisposed to dusrhythmias |
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signalment of aortic atenosis
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genetically transmitted in Newfoundlands
other breeds predisposed: boxers, goldners, rotties, GSD, and GSHP |
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aortic stenosis is an incidental finding during the first vaccination just like in ____________
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PDA
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when do murmurs and lesions sometimes develop with aortic stenosis
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three months or so of age
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at what age can a dog be certified that it is free of congenital heart disease
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12 months
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what are the most common signs of aortic stenosis
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syncope or sudden death due to arrhythmias. it is rare for dogs to develop left sides HF signs
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where is the systolic murmur heard the loudest in aortic stenosis
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over the left heart base, radiating up the carotids in the neck and to the right nemithroax
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diagnostics for aortic stenosis
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radiographs
angiocardiography echo m-mode doppler catheterization |
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radiographic findings for aortic stenosis
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often normal
concentric hypertrophy hard to see may see dilation of the descending aorta with left ventricular and atrium enlargement |
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what findings are seen for aortic stenosis when using echo
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concentric hypertrophy of the ventricles
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treatment of aortic stenosis
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medical treatment is palliative
beta blockers recommended in dogs with syncope, moderate to severe gradients, ventricular arrhythmia or ST segment changes beta blockers must be used with caution class 1 antiarrhythmics (lidocaine, mexiletine, procanamide) should be used with care. sotalol is better choice for ventricular arrhythmias surgery = does not increaase surviva if HF--diuretics, vasopressors... |
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why are positive ionotropes contraindicated in aortic stensois treatment
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they may exacerbate the arrhythmia and increase MVO2
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prevention of aortic stenosis
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beta blockers to prevent progression = controversial
do not breed |
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aortic stenosis prognosis
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it is progressive and progression is rapid in young dogs
can die suddenly control of infection is important |
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DDX aortic stenosis
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continuous murmurs
other causes of syncope physiological murmurs bacterial endocarditis of the aortic valve |
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what is the third most common congenital cardiac disorder in the dog
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pulmonic stenosis
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T/F: pulmonic stenosis is common in the cat
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false--rare
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name the three types of pulmonic stenosis
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subvavular
valvular (most common) supravalvular |
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pathophysiology of pulmonic stenosis
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obstruction to ejection results in concentric hypertrophy of the right ventricle. there is a post stenotic dilatation of the main PA truck due to the high velocity blood flow. the right atrium is enlarged due to increased pressure in the ventricle. ventricle is enlarged too.
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signalment of pulmonic stenosis
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most common in english bulldog, scottish terrier, and wirehaired for terrier.
polygenic inheritance in the beagle |
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signs of pulmonic stenosis
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only seen in those with severe lesions, but even then only 35% develop signs.
exercise intolerance and inactivity, weakness, syncope, sudden death, right sided CHF with concurrent tricuspid dysplasia |
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describe the murmur you hear with pulmonic stenosis
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systolic heart murmur over the left heart base that radiates to the right and up the neck.
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diagnostics for pulmonic stenosis
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rads
echo M mode doppler aniopathy catheterization ECG |
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what do you see on radiographs of pulmonic stenosis
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right ventricular enlargement with pulmonary trunk dilation and maybe signs of right sided heart failure
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what do you see on echo with pulmonic stenosis
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right ventricular hypertrophy, flattened septum, large right atrium, malformed pulmonic valve and dilation of the pulmonary trunk
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treatment of pulmonic stenosis
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balloon valvuloplasty recommended for moderate to severe stenosis
atenolol when surgery not possible |
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T/F: pulmonic stenosis is an incidental finding at the first vaccination
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true
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normal velocity of blood flow across the pulmonic valve
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1.2m/s
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what speeds of blood flow across the pulmonic valve indicate pulmonic stenosis
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anything over 1.2m/s
>4-5 = severe 3.5v= mild |
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prevention of pulmonic stenosis
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do not breed
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prognosis of pulmonic stenosis
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good in mild cases
uncertain in moderate cases 30% of the 35% dogs with severe pulmonic stenosis thatshow signs die suddenly |
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DDX for pulmonic stenosis
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subaortic stenosis
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pathophysiology of VSD
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small openings may have little effect
large openings blood move from LV to RV (high to low pressure) most occur high up in the membranous part of the septum and thus blood flow goes from LV to PA. this causes volume overload of the LV and eccentric hypertrophy and left CHF |
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T/F: VSD are common in cats
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true
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T/F: VSD are common in dogs
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False--uncommon
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name two dog breeds reported to get VSD
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english bulldog
keeshond |
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signs of VSD
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small VSD = incidental finding
larger defects = stunted growth, may see signs of left sided CHF systolic murmur over the right sternal border and there may be a palpable thrill may see signs of left sided CHF |
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diagnostics for VSD
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rads
echo doppler angiopathy ECG |
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signs of VSD on radiographs
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prominent pulmonary vessels due to pulmonary overcirculation
left heart enlargement large VSDs and R-L shunts may cause right heart enlargement |
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on echo what must VSD be differentiated from
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septal drop out which is a common artifact
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what diagnostic test provides the definitive diagnosis for VSD
|
Doppler
can be used to calculate the size of the defect |
|
|
treatment of VSD
|
small VSDs = no treatment needed
severe VSDs = surgery (synthetic patch, pulmonary banding); arterial vasodilators may reduce degree of L-R shunting |
|
|
prevention of VSD
|
do not bred
|
|
|
prognosis of VSD
|
mild to moderate VSD = good to excellent
poor if R-L shunting and pulmonary hypertension develops |
|
|
T/F: occasionally the VSD can spontaneous close
|
true
|
|
|
what is seen defect wise in tetrology of fallot (TOF)
|
pulmonic stenosis
over riding aorta VSD hypertrophy of the RV |
|
|
pathophysiology of TOF
|
blood flows from the LV to the RV through the VSD during systole = mild case
severe cases:(more common) flow is R-L due to higher pressure in the RV. deoxygenated blood is pumped into systemic circulation and cyanosis and erythrocytosis develops. rare to see CHF RV hypertrophy predisposes the arrhythmias |
|
|
signalment of TOF
|
autosomal recessive in the Keeshond
|
|
|
signs of TOF
|
stunting, exercise intolerance, shortness of breath, and syncope
murmur usually heard at first vaccination and most patients are cyanotic |
|
|
diagnostics for TOF
|
rads
echo doppler angiography catheterization ECG |
|
|
what do you see on rads with TOF
|
right heart enlargment and small pulmonary vessels
|
|
|
what is seen on echo with TOF
|
right ventricular hypertrophy, overriding aorta, pulmonic steonsis
|
|
|
what do you see on doppler with TOF
|
increased peak flow across the pulmonary valve and a R-L or L-r shunt through the VSD
|
|
|
what does angiography identify in TOF
|
VSD
RV hypertrophy pulmonic stenosis direction of the shunt |
|
|
treatment of TOF
|
surgery is variable with success
medical therapy is empiraical--control arrhythmias and heart failure. beta blockers benefit some patients. hydroxyurea and/or periodic phlebotomy will lower the HCT and hyperviscosity low dose aspirin might prevent thromboembolism |
|
|
what type of drug is contraindicated in TOF
|
vasodilators
|
|
|
prevention of TOF
|
do not breed
|
|
|
prognosis of TOF
|
depends on the severity
|
|
|
DDX for TOF
|
other causes of cyanosis
|
|
|
in what direction does blood flow in a large ASD
|
into the RV since it is more distensible due to its thinner walls
|
|
|
what happens to the RV in ASD
|
RV enlargement (also the pulmonary vessels are enlarged)
|
|
|
which diagnostic is best for ASD
|
Doppler
|
|
|
if a murmur is heard in ASD what might it be due to
|
relative pulmonic stenosis
relative tricuspid valve stenosis splitting of the second heart sound |
|
|
T/F: most dogs are symptomtic when they have small ASD
|
False--most a asymptomatic and signs are seen with large defects
|
|
|
ASD treatment
|
standard HF treatment
surgery |
|
|
what is the most common congenital malformation in cats and large breed dogs are predisposed to it
|
AV valve malformations
|
|
|
lesions of AV valve malformation
|
thickened or fused valves
malpositioned, partially developed, or absent papillary muscles too long, short or absent chordea tendinae |
|
|
what does signs associated with AV valve malformations depend on
|
the valves involved and if there is valvular insufficiency or stenosis
|
|
|
treatment of AV valve malformation
|
palliative
furosemide and and ACE inhibitor mostly arterial vasodilators may be helpful |
|
|
pathophysiology of AV valve malformation
|
stenotic valves decrease ventricular filling which may result in increased atrial pressure and signs of CHF
|
|
|
name and describe the congenital disease mainly seen in Burmese and Siamese cats
|
endocardial fibroelastosis
fibrosis of the ventricular endocardium leads to stiffening of the LV and eventual dilation and failure |
|
|
what is DCM in the canine (describe)
|
common in giant and large breed dogs
characterized by progressive dilation of the left and/or right ventricle with mild thinning of the ventricular walls resulting in decreased myocardial contractility resulting in decreased CO and neuroendocrine activation |
|
|
what are some historical lesions associated with DCM
|
absence of inflammation
attenuated wavy myofibers fibro-fatty infiltration loss of myocytes myocardial fibrosis |
|
|
T/F: DCM is idopathic but also decreased cases with an unknwon but apparent genetic etiology
|
true
|
|
|
three stages of DCM progression
|
arrhythmogenic cardiomyopathy (ACM)
occult phase classic DCM |
|
|
Describe ACM
|
dogs may have arrhythmias but normal LV contractility
wolhounds may presentwith lone AF and dobes with only VPDs |
|
|
describe the occult phase of DCM
|
animals appear normal to the ownners but have morphological changes and a trend towards decreased contractility
ventricular arrhythmias or AF are common lasts 2-4 years in dobes |
|
|
what are the morphological changes seen in the occult phase of DCM
|
mainly LV enlargement and thinning of the walls of the ventrcile
|
|
|
describe classic DCM
|
dogs that have it are in heart failure (mostly left)
also have ventricular arrhythmias or AF |
|
|
signalment for DCM in the dog
|
giant breeds(irish wolfhound, scottish deerhound, great dane) and large breed dogs (dobes, boxer, st. bernard, afghans, newfies, old english sheepdogs)
most common in middle aged males |
|
|
signs of canine DCM
|
sudden death from arrhythmias occurs in about 30% of cases
may be signs of weight loss, exercise intolerance, weakness, syncope, dyspnea, orthorpnea, coughing, restlessness at night and abdominal distension poor BCS, signs of left or right heart failure, muffledheart and lungsounds, signs of AF, systolic murmur, gallop sounds are common |
|
|
diagnostics for canine DCM
|
lab
rads echo m mode doppler ecg |
|
|
lab results for canine DCM
|
pre renal azotemia
increased liver enzymes low blood taurine or carnitine hyptoT4 in affected dobes |
|
|
radiographic findings in canine DCM
|
heart enlargement (left heart can predominate)
|
|
|
which diagnostic test provides the definitive diagnosis for canine DCM
|
echo
|
|
|
what signs are seen on Echo in dogs with DCM
|
decreased fractional shortening
LV and LA enlargement with flabby ventricular walls in dobes a LV internal diameter in systole >38mm and LVIDd of 46mm is suggestive |
|
|
in most dogs with DCM what is the fractional shortening
|
>25%
|
|
|
ECG findings for canine DCM
|
VPDS
AF signs of left or right heart failure depressed ST segement |
|
|
treatment of ACM
|
lone AF:
beta blockers (atenolol or metoprolol) titrated diltiazem very effective in controlling HR but does not confer the cardioprotection of beta blcokers digoxin not effective at controlling lone AF ventricular arrhythmias treat if c/s antiarrhythmis in those without c/s beta blockers to control VPDs VT = sotolol or combo of mexiletine and atenolol |
|
|
treatment of occult DCM
|
ACE inhibitors in dobes seem to delay onset
beta blockers may have similar affect treat arrhythmias monitor |
|
|
essentials for treating DCM in dogs
(read that section) |
supplemental O2
symptomatic treatment control pulmonary edema using furosemide improve contractility with pimobendan ACE inhibitors at max dose to blunt the RAAS response control arrhythmias |
|
|
prevention of canine DCM
|
age of onset is variable
annual echos and Holter monitors can be done annually on at risk breeds genetic markers should be available to detect at risk animals and enable breeding programs to eradicate the disease |
|
|
canine DCM prognosis
|
guarded to poor with therapy generally markedly increasing quality of life
ACE inhibitors and pimobendan increase life expectancy up to 350 days cocker spanials seem to recover in 2-4 months of therapy with taurine and carnitine for DCM |
|
|
DDX for DCM
|
pericardial effusion
|
|
|
what is the most abundant free amino acid in the tissues
|
taurine
especially in the muscle, viscera and brain |
|
|
T/F: taurine is an essential amino acid in the dog
|
false--it is in cats b/c they cannot synthesize it
|
|
|
what cardiomyopathy can taurine deficiency be seen in
|
DCM
|
|
|
______ are conjugated almost exclusively with taurine
|
bile acids
|
|
|
taurine is an important moderator of _________
|
calcium flux--it reduces platelet aggregation, stabilizes neural membranes and is a positive ionotrope
|
|
|
what diets are dogs on when a taurine deficiency is noted
|
lamb and rice or vegetarian
|
|
|
how is taurine deficiency associated with DCM
|
unknown
|
|
|
T/F: dogs that have DCM and are not of the predisposed breeds should be given taurine
|
true
(especially Goldens) |
|
|
what breeds of dogs with DCM would you given taurine supplemented with carnitine
|
boxers and cocker spaniels
|
|
|
how is DCM characterized in cats
|
ventricular dilatation, apparent thinning of the ventricular walls and decreased contractility
|
|
|
what are the majority of cats of DCM in cats due to
|
taurine deficiency
|
|
|
signalment of DCM in cats
|
middle aged to older males with Burmese, Siamese or Abyssinaian breed predisposed
|
|
|
signs of feline DCM
|
acute onset of paresis/paralysis due to thromboembolism
dyspnea, anorexia, lethargy, sometimes vomiting hypothermia, weak femoral pulses, poor CRT muffled heart and lung sounds gallop rhythms and murmur |
|
|
what sign in feline DCM are suggestive of taurine deficiency
|
focal retinal degeneration
|
|
|
feline DCM diagnostics
|
lab tests
rads echo M mode doppler ECG |
|
|
lab abnormalities in feline DCM
|
low serum taurine
increased T4 if hyperthyroidism is present |
|
|
radiographic signs of feline DCM
|
pleural effusion
diffusely enlarged heart may see diffuse alveolar and interstitial patterns |
|
|
what is the definitive diagnostic test for feline DCM
|
echo
|
|
|
feline DCM treatment
|
treat pulmonary edema/pleural effusion with O2, furosemide, venodilators (NG cream) and thoracocentesis
ACE inhibitors may improve systolic function dobutamine infusion can give digoxin if needed treat thromboembolism if occurred or prevent with aspirin or coumarin supplement taurine treat hyperT4 is present |
|
|
feline DCM prognosis
|
poor if not due to taurine deficiency
|
|
|
DDX for feline DCM
|
HCM
|
|
|
In __________ there seems to be a functional abnormality of the myocytes that leads to increased cell stress and activation of trophic and mitotic factors --> papillary muscle and LV concentric hypertrophy
|
HCM
|
|
|
what does HCM look like microscopically
|
myocytes are enlargd and there is fiber disarray as a result of abnormal branching
|
|
|
T/F: most cats do not develop clinical signs as a result of HCM
|
true
|
|
|
pathophysiology of HCM
|
LV lacks compliance which impairs relaxation and filling in diastole. chamber size is reduced and almost non existent in systole. systolic function is preserved but there may be outflow tract obstruction. mitral insufficiency can occur and a murmur can result.
stasis of blood in the LA predisposes to thrombus formation. dislodge and go to the bifurcation of the aorta (ATE) |
|
|
HCM signalment
|
middle aged male cats
|
|
|
HCM signs
|
many are asymptomatic
murmur is incidental finding some have syncope/collapse or sudden death due to arrhythmias may see LCHF Gallop rhythm and systolic murmurs are common ATE = paralysis of hind limbs, cool to touch, painful. can mimic HF signs so do a rad |
|
|
diagnostics for HCM
|
exclusion diagnosis (rule out other causes of hypertrophy first)
biomarkers in blood muscle necrosis and elevated CK and AST with ATE Imaging (rads, echo, M mode, etc) ECG |
|
|
radiographic findings in HCM
|
LA enlargement
variable LV enlargement valentine shaped heart may see pulmoanry edema if there is CHF |
|
|
Echo findings for HCM
|
marked thickening of the interventricular septum and/or LV walls, reduces LV lumen, enlarged LA
sometimes can see LVOT obstruction |
|
|
what diagnostics can be used to confirm ATE associated with HCM
|
Angiography
scintigraphy doppler |
|
|
HCM treatment see packet
|
See packet
|
|
|
Prevention of HCM
|
do not breed
|
|
|
HCM prognosis
|
asymoptomatic cats = guarded to good
worse prognosis if have more diffuse or regioanlly diffuse hypertrophy extremely poor = heart failure, ATE |
|
|
what is the key prognostic factor for HCM
|
LA size
|
|
|
explain HyperT4 in the feline and how it is related to heart enlargement
|
cats with hyperT4 may have LV concentric hyptrophy. most hoever have eccentric hypertrophy resulting from high output state and volume overload
|
|
|
when does restrictive cardiomyopathy occur in the cat
|
when there is endocardial, subendocardial or myocardial fibrosis or infiltrative disease that reduces diastolic filling
|
|
|
restrictive cardiomyopathy signalment
|
middle aged to older cats
|
|
|
what might restrictive cardiomyopathy result from
|
myocarditis but in some cases it is a late stage of HCM.
|
|
|
late stage of HCM
|
restrictive cardiomyopathy
|
|
|
what occurs commonly with restrictive cardiomyopathy
|
thromboembolism and arrhythmias
|
|
|
restrictive cardiomyopathy treatment
|
furosemide
ACE inhibitors diltiazem beta blockers |
|
|
prognosis of restrictive cardiomyopathy
|
poor
|
|
|
familial disease in boxers
|
ARVC, boxer cardiomyopathy, FVA
|
|
|
etiology of boxer cardiomyopathy
|
unknown
|
|
|
What are there low levels of in boxer cardiomyopathy and what do these levels indicate
|
connexin 43 and calstabin
indicates dysfunction of gap junctions and leaking of calcium from the SR |
|
|
boxer cardiomyopathy signalment
|
boxers
1-15 years most are 6-10 |
|
|
boxer cardiomyopathy signs
|
normal PE but can hear VPDs
history of sudden death, no abnormalities, weakness, syncope signs of RCHF |
|
|
definitive diagnosis for boxer cardiomyopathy
|
PM in animals with sudden cardiac death
probably diagnosis in live animals is based on family history, VT, histroy of episodes of weakness/syncope |
|
|
______ concentrations are higher in dogs with boxer cardiomyopathy and are directly proportional to the number of VPCs/24hrs
|
cTn-1
|
|
|
detection of VTA in boxer cardiomyopathy
|
holter monitor >100is highly suggestive of boxer cardiomyopathy
|
|
|
what does chest x-rays and US look like in boxer cardiomyopathy
|
normal
|
|
|
boxer cardiomyopathy treatment recommendations
|
recommended to treat dogs with episodic weakness and syncope and asymptomatic dogs that have over 100 VPDs a day, episodes of VT or the R on T phenomenon
|
|
|
boxer cardiomyopathy treatment
|
sotolol or combinationof mexiletine and atenolol are used most commonly
monitor treatment with holter monitor |
|
|
possible consequence of boxer cardiomyopathy treatment
|
proarrhythmic effect and there is an increase in C/S or number of VPDs or their complexity
|
|
|
boxer cardiomyopathy prognosis
|
sudden death is possible
|
|
|
in boxer cardiomyopathy who are c/s more likely seen in
|
dogs with large numbers of VPDs and those with episodes of VT
|
|
|
boxer cardiomyopathy prevention
|
screen at a year of age for subaortic stenosis by US and for ARVC by holter monitoring and thereafter every year for ARVC
if a dog produced affected dogs do not use him/her again |
|
|
boxer cardiomyopathy:
<20 VPDs = 20-100VPDs = 100-300VPDs = |
1. if appears normal can breed
2. suspicion of disease, re-evaluate in year 3. suspicious of disease, withhold from breeding until next screening in a year |
|
|
DDX boxer cardiomyopathy
|
DCM
SAS |
