Cardiac disease Flashcards
Normal heart function
The amount of blood entering the heart (pre-load) should equal the amount of blood exiting the heart (after-load)
If more blood is trying to enter the heart than is leaving it, that could cause a damming effect and higher pressure “upstream”
Each contraction of the heart should result in the maximum volume of blood being pumped out. If there is insufficient blood being pumped out of the heart; this may result in lack of tissue perfusion. Lack of perfusion means tissues may not receive adequate oxygen and nutrients and removal of waste products will be impaired.
Effusion
Fluid in 3rd space
Pulmonary edema
Fluid accumulate in alveoli. Prevents oxygen uptake
Pleural effusion
- fluid around the lungs; prevents filling with air
Abdominal effusion
Fluid in the abdomen
Ascites
Clear fluid in the abdomen
Primary cardiac disease
When something goes wrong with the heart itself
Congenital or inherited, traumatic, degenerative
Secondary cardiac disease
When something goes wrong elsewhere in the body that affects the heart, or puts additional strain on the heart
Systemic disease, infection, toxicity, metabolic, secondary to lung disease
Causes of secondary heart disease
Systemic disease
Hyperthyroidism, renal disease, neoplasia, pulmonary disease
Infection
Periodontal disease, neonatal septicemia, heartworm, hardware disease
Toxicity
Digitalis, arsenic, snakebites
Metabolic
Copper and selenium deficiencies
Prognosis of cardiac disease
Depends on the cause
Rate of progression of disease is variable
Depends on the severity of disease
Prognosis decreases once c/s are present
Secondary damage to other organs/tissues
Left untreated it will eventually progress to heart failure
Top 4 cardiac diseases
Mitral valve insufficiency (dogs/horses)
Hypertrophic cardiomyopathy (cats)
Dilated cardiomyopathy (dogs)
Endocarditis (cattle)
Who is most susceptible to cardiac disease
Old dogs
Main coons
Cavalier king charles
Heartworm
Typical presenting complaint of cardiac disease
Syncope (fainting spells) looks similar to a seizure
Weakness
Open mouth breathing in cats
Coughing
Exercise intolerance
LA: decreased production, weight loss, fever
Animals are often asymptomatic at the time of diagnosis, or only subtle signs are present
Tachycardia
Increased HR
Bradycardia
Decreased HR
Arrhythmia
irregular heartbeat due to problems with the sinus node or conductivity
Murmurs are described by
“Whooshing” sound= turbulence
Describing murmurs
How loud?
Grades 1-6
Where are they the loudest (left or right side, same, which rib space)
Associated with systolic or diastolic
Has it changed over time
Diagnostics used for heart disease
Echocardiogram (echo)
Ultrasound of the heart- most accurate
Radiographs
Electrocardiogram (ECG=EKG)
Blood pressure measurement
Taurine deficiency can cause
Cats can get DCM if eating a taurine deficient diet
Dogs can get taurine from other amino acids
Except for certain lineages AM Cocker spaniels
Possibly golden retrievers
Source of taurine
Insects
Raw Meat- birds, seafood
Commercial cat food (250-500 mg/day)
DCM pathology
Acquired
Pathology
Problem with the cardiac muscles; weakness over time
Heart muscles becomes distended, flabby, weak
Left side of the heart usually affected first; followed by right side
Outline of the heart becomes larger and rounded and the ventricles are enlarged
As the muscles continues to stretch
The conductive fibers become spread out, and mya lose their ability to coordinate muscle contraction
Cardiac vessels become spread out and areas od the heart may have less perfusion
Pump becomes less effective (decreased stroke volume
Decreased peripheral perfusion
Clinical signs of DCM
Weakness, lethargy, exercise intolerance, cough, syncope
Some dogs do not show signs of clinical disease until they are already into heart failure
Sudden collapse
Treatment for DCM
Goals of treatment are
Increase strength of heart muscle- to help the heart get stronger and increase cardiac output
Decreased heart rate-prevent heart from tiring out
Prognosis for DCM
Progressive
Cannot reverse heart muscle damage
May die from lack of tissue perfusion or the heart muscle gives out
Or, the disease will eventually progress to congestive heart failure with pulmonary effusion
Death can be sudden
Non-hereditary DCM can be caused by
2018–FDA Investigation began because DCM was being diagnosed in breeds not typically predisposed to the condition
Sometimes multiple dogs within the same household
Pathophysiology not yet completely understood
Associated with diets containing legumes or potatoes as main ingredients (grain free diets)
Believed to be linked to taurine
Hypertrophic cardiomyopathy is caused by
Primary HCM- inherited in cats
Myosin mutation
Secondary to hyperthyroidism in cats
Secondary to mitral valve disease in dogs
Can be secondary to any disease that makes the heart work harder
The heart is a muscle; muscles grow when they are exercised
Sequelae is
Thickening of the LV muscle
Decreased filling space
Less blood pushed out per pump (decreased cardiac output) AND
Back-up of blood to atria
Back up of blood to veins
Heart muscle outgrows its own blood supply
Increased risk of clot formation (cats)
Because less blood exits the heart each time it pumps, the heart has to beat faster…..once this disease starts, it is chronic, progressive, and makes itself worse over time
Presenting and clinical signs of hypertrophic cardiomyopathy
Exercise intolerance, syncope
Swollen (belly,limbs)
ADR= “ain’t doing right”
Hind end weak or paralyzed
Open mouth breathing, struggling to breathe
Cyanosis
Sudden collapse
IF THE BOTTOM THREE ARE SHOWN IT IS AN EMERGENCY
Goals of treatment for hypertrophic cardiomyopathy
Treat the underlying condition
Decrease the workload on the heart
Keep blood pressure within normal limits
Prevent thromboemboli
Death by HCM is caused by
Pleural effusion and pulmonary edema inhibit gas exchange
Heart outgrows its own blood supply
Clots block blood flow back to heart or to the brain
Lack of tissue perfusion
Endocardiosis
degenerative thickening
Dogs, horses
Endocarditis
Inflammatory; may or may not be infectious
Cattle
Bacterial endocarditis in cattle primary causes
A secondary cardiac condition
Primary causes include
Metritis (inflammation of the uterus)
Mastitis
Foot or liver abscesses
Septic arthritis
Traumatic reticular peritonitis
Long term indwelling catheter
Bacterial endocarditis in cattle clinical signs and PE findings
Weight loss
Anorexia
Heart murmur
Decreased production
Fever
Sudden death
Mitral valve insufficiency/regurgitation is common in
Mitral valve endocardiosis
Endocardiosis = degenerative
Dogs and horses
Older animals
Dogs: smaller breeds, males, overrepresented
Mitral valve regurgitation is
Backflow/leaking of blood into LA
Turbulence = murmur
Heart pumps harder → secondary thickening of heart muscle
Heart failure is characterized by
When the heart can no longer pump to meet the demands of the tissues
Heart can’t pump enough blood, so there is a backup that occurs = Congestive HF
Many underlying causes of HF
Subclinical HF is
Aka asymptomatic HF
Heart does not pump effectively
No clinical signs
Patient may not be aware of changes in body
Compensatory mechanisms help maintain BP
Blood vessels constrict
Body retains water
Keeps tissues perfused
Start treatment when heart enlargement is detectable on radiographs - FOR LIFE
Clinical HF is
Patient has clinical signs
Clinical signs appear because compensation is no longer enough to maintain normal blood flow through the heart to the rest of the body
Additional medications indicated at this point if owner is willing
Pathology of clinical HF
Decreased output from the heart
This caused decreased perfusion of tissues
Clinical signs
Syncope
Weakness, exercise intolerance
May lead to tissue/organ damage (especially kidneys)
Back up BEFORE the heart
Be able to explain what can happen when there is increased preload
What happens in LEFT sided congestive HF
Pulmonary edema in left sided HF
Fluid in alveoli
Clinical signs are related to respiration
Open mouth breathing
Struggling to breathe
Cyanosis
Shallow, rapid respiration
What happens in RIGHT sided congestive HF
Liver in RSHF → may develop liver failure
Abdominal distension due to ascites
Note that the animal is otherwise cachexic (can see the ribs and dorsal column)
Treating HF
Rest, restricted activity/excitement
Reduce salt intake
Vasodilators- Dilate blood vessels (decrease BP)
Diuretics- to increase urination (decrease BP)
Drugs to slow down heart to prevent arrhythmias
Preventing thromboemboli
Prognosis of HF
Guarded - ALWAYS progressive
Will eventually lead to death d/t:
Pulmonary edema +/- pleural effusion
Output failure
Arrhythmia may or may not be present
Cardiac infarct
