Dogs and Cats 23 Flashcards
A-V blocks what are the 3 degrees and what occurs
○ First degree - prolonged PR interval
○ Second - intermittent AV conduction
○ Third degree - complete AV block with escape rhythm and no relationship between P and QRS - AV dissociation
Approach to A-V blocks what need to rule out and what is priamry cardiac
i. Rule out drug administration, electrolyte disturbance - especially for first degree blocks
ii. If primary cardiac, often not structural - CANNOT FIX
□ Long-term anti-cholinergic may help if positive response to test
□ Pacemakers
® Good long-term response
® Better if no CHF
® Some mild complications
® Expensive
A-V block when to determine whether vagal stimulated, what treat with and causes
□ To determine whether vagal -> Administer atropine (0.04 mg/kg IV) and repeat ECG 10-15minutes later ® If HR increase by 100% or > 140 bpm = vagal ® If P rate increase but QRS doesn't = not vagal ® If in between repeat test ® If no change P than atrial standstill ® SSS variable response □ Causes of excess vagal tone ® Chronic respiratory disease ® GI disease ® Hypothyroidism ® Ocular or retrobulbar disease ® CNS (increase intra-cranial pressure)
what are some important points to remember about A-V blocks
§ In AV blocks if the conduction system is OK high up in the ventricular conduction system the more normal the QRS looks
§ AV blocks can be due to structural disease - BUT OF THE CONDUCTION SYSTEM NOT USUALLY THE MYOCARDIUM
§ Generally if treating a tachyarrhythmia we don’t want to also decrease heart contractility
congenital cardiac disease classification, what do they cause and main types in dogs and cats
Classification
- Arteriovenous shunts
- Failure of normal valve development
- Incomplete separation or mal-positioning of great vessels
- NEARLY ALWAYS cause murmur BUT DON’T ALWAYS cause congestive heart disease
○ Intensity of murmur not related to how bad it is
Types
- Dogs: patent ductus arteriosus (PDA) -> pulmonic stenosis (PS)/ Aortic stenosis (AS)
- Cats: AV dysplasia/VSD
Extra-cardiac shunt = PDA signalment and pathophysiology
- Common in dogs
- Females > males
- Genetic predisposition some breeds
- What occurs
○ PDA diverts foetal blood from PA into aorta
§ Aorta pressure > PA pressure in diastole and systole so LEFT TO RIGHT SHUNT at all stages of cardiac cycle when born
□ Unless there is pulmonary hypertension (reverse PDA)
○ Increased venous return from lungs
§ Volume overload on LA and LV - dilation and hypertrophy
○ Increased after-load on RV
§ Concentric hypertrophy (not as significant as left-side)
○ Aneurysm (bulge) in descending aorta
○ If pulmonary hypertension
§ PA pressure > aorta pressure so R to L
□ Usually very large shunt so resistance to flow
PDA clinical signs when not and when often clinical and then what occurs
○ Often not clinical, but may show fatigue or poor growth
§ CHF develops within 6 - 12 months if it is going to at all
○ With right-left shunts - reversal
§ Due to pulmonary hypertension
□ Consequence of PDA
□ Occurrence congenital or acquired pulmonary disease
§ Chronic hypoxia leads to polycythaemia (massively increased PCV and hyperviscosity) -> seizures
§ Murmur may get softer
§ May not heart murmur
○ Differential cyanosis - may occur
§ Caudal part of the body blood supply occurs as shunting occurs so deoxygenated blood at this point
§ Cranial part of body supplied by brachycephalic trunk branches off aorta BEFORE PDA -> oxygenated blood
What are the 2 main clinical findings with a PDA
1) Continuous (machinery) murmur detected at vaccination
§ Aortic pressure is always greater than PA pressure systole and diastole
§ Precordial thrill at left heart base - may be able to feel
2) Widened pulse pressure
Low aortic diastolic pressure
What are the 3 main ways to diagnose a PDA
○ Clinical findings - continuous murmur over left side in puppy - not much else can do this
○ Radiography
§ Lateral - cardiac enlargement, especially LA, pulmonary over-circulation, CHF if severe
§ DV - triple bulge: PA, aorta, L auricle
○ Echocardiography - can see the shunt and enlarged left atrium
What are the first 3 types of PDA, what occurs, diagnose and treatment
○ Type 1 - small PDA
§ Generally asymptomatic L -> R shunt
§ X-ray normal at 1-2 years
§ Surgery not urgent but recommended for normal life span
○ Type II - medium PDA
§ Asymptomatic L -> R shunt with continuous murmur and thrill L heart base and also audible at L apex (mitral regurgitation due to LV dilation) and normal-bounding pulse
§ Mid-moderate heart enlargement < 1 year old
§ Surgery recommended, but can wait a few weeks
○ Type III a - large PDA prior to CHF
§ Usually decreased exercise tolerance with continuous murmur and thrill present over most of the left thorax and often MR murmur at L apex with bounding pulse
§ Marked heart enlargement < 6 months old with significant increase in pulmonary vascular marking
§ Surgery recommended without delay
What are the last 2 types of PDA what occurs, clinical signs and treatment
○ Type III b - large PDA plus CHF
§ All of IIIa feature PLUS dyspnoea due to pulmonary oedema
§ Often in poor body condition and may have atrial fibrillation
§ Treat medical conditions prior to surgery as soon as stable
○ Type IV - large PDA plus pulmonary hypertension
§ R -> L or balanced shunt
§ May show weakness or collapse with exercise (can present from 2 weeks to 12 years)
§ NO SURGERY (contraindicated due to pulmonary hypertension), treatment is medical (phlebotomy, hydroxyurea) to decrease PCV
Treatment for PDA and prognosis
- Surgery
○ Methods of ligation
§ Surgical ligation - requires thoracotomy so some risk and post-op chest drain
□ Haemorrhage possible but recovery good
§ Coil embolization - transvenous using fluoroscopy - better probably
○ Restrict exercise one month post-op - Prognosis
○ Much better if corrected
○ Concurrent MR worsens prognosis
○ Age at which closed or presence of CHF does NOT worsen prognosis
○ Individual variation
Pulmonic stenosis types, how common in dogs and what occurs
- Valvular, sub-valvular or supra-valvular
- Relatively common in dogs
○ English bulldogs (male)
○ Boxers
○ Beagles (inherited)
○ Small breeds - What occurs
○ Reduced diameter of RVOT (right ventricular outflow tract)
§ Increased after-load
§ Concentric hypertrophy
○ Post-stenotic dilation as blood increases in velocity - why hear murmur
Pulmonic stenosis clinical signs
○ Incidental murmurs
§ Ejection murmur LEFT HEART BASE
§ Normal femoral pulses
§ 10% have diastolic murmur as well
○ Exercise fatigue, weakness and syncope if severe
○ Rarely get RSCHF unless concurrent tricuspid dysplasia
Pulmonic stenosis diagnosis
○ Clinical findings
○ ECG
○ Radiographs
§ DV gets reverse D with pulmonary trunk bulge due to dilation
§ RV enlargement
§ Contrast angiography
○ Echocardiogram
§ Needed for severity assessment and diagnosis
§ RV hypertrophy and RA dilation
§ Narrowing at pulmonic valve
§ Measure velocity and convert to pressure gradient for treatment recommendations
Pulmonic stenosis when to treat
○ Pressure gradient > 80mmHg
§ Increased risk of syncope/sudden death
§ Treatment currently recommended
○ Pressure gradient 50-80 mmHg
§ Asymptomatic but long-term prognosis poor
○ Pressure gradient < 50mmHg
§ Mild stenosis so don’t really require treatment
○ May live a normal life span if no clinical signs - NO BREEDING
○ IF there is RSCHF due to concurrent tricuspid dysplasia then treatment may be beneficial regardless of severity
Pulmonic stenosis treatment options
○ Closed patch graft
○ Closed valvulotomy
○ Balloon dilation (valvulopasty) - most recommended
§ Down the jugular and then dilate
§ Best response if CHF at time of diagnosis
§ Some associated mortality
§ Still have increased pressure gradient
Aortic stenosis which most common, breeds and pathophysiology
- SAS most common
○ Fibrous ring of tissue immediately below aortic valve - Newfoundlands, boxers and goldern retrievers
- Pathophysiology:
○ Increased after-load on LV
§ Concentric LV hypertrophy
○ Flow becomes turbulent distal to the stenosis
§ Post stenotic dilation
○ Coronary arteriosclerosis and myocardial necrosis/fibrosis develops
Aortic stenosis clinical signs
○ Exertional syncope and sudden death
§ Bradycardia secondary to increased LV systolic pressure and vasodilation
§ Arrhythmias usually secondary to haemodynamic changes
○ Not many get LSCHF
○ Murmur may be incidental
§ L base but pulses will be weaker
§ To and fro if also insufficiency
§ Takes time to develop as hypertrophy progresses
§ Not clear about severity until > 12 months
Aortic stenosis diagnosis
○ Physical examination ○ Radiography § LV enlargement and post-stenotic dilation ○ Echocardiography - gold standard § LA enlargement and dilation of ascending aorta § LV hypertrophy § Turbulence Measure velocity across aortic valve
Aortic stenosis treatment
○ Not indicated for mild disease
○ Prophylactic antibiotics
○ Exercise restriction
○ Beta-blockers
○ Balloon dilation
§ Very technically demanding - cannot go through jugular
§ No evidence actually prolongs survival
§ May be helpful if CHF due to concurrent MVD
AV valve malformations what are the 2 main ones, what common in and what result in
- Same as acquired valvular disease - same treatment
1) Tricuspid
○ Part of multiple defects in cats
○ Large-breed dogs
○ Labradors
○ Usually insufficiency due to fusion of chordae or thickening of leaflets
2) Mitral
○ Very common sole or as part of ecd in cats
○ Large-breed dogs
○ English bull terrier
○ Usually insufficiency not stenosis
Tetralogy of fallot how common and consists of
- Uncommon ( cat < dog)
- Consists of:
○ High VSD
○ Pulmonic stenosis
○ Overriding aorta
§ Dextroposition
○ RV hypertrophy
§ Compensatory
Pulmonary hypertension diagnosis and treatment
Diagnosis
- Often one of suspicion NOT conformation
- Echo can show signs of increased RV outflow obstruction (increased PA velocity; tricuspid regurgitation)
- Echo can be normal
Treatment
- Treat underling cause if possible
○ Heart worm or pulmonary oedema
- Phosphodiesterase inhibitors at the moment main stay of treatment - if above not effective
○ Pimobendan
○ Sildenafil - vigra - vasodilator - only if pimobendan doesn’t work by itself
○ Theophylline
Systemic hypertension what is it and causes with most common and not common
- Persistently high arterial blood pressure (BP)
- BP = CO x TPR
- BP = (HR x SV) x TPR
- Very important disease of cats
Causes - Primary
- Secondary
○ Renal disease - MOST COMMON
○ Cardiac disease
○ Hyperadrenocorticism
○ Hypokalaemia
○ Diabetes mellitus (dogs not cats)
○ Acromegaly
○ Polycthaemia
○ Pheochromocytoma
○ Hyperthyroidism - NOT COMMON - If have hypertension with hyperthyroidism then probably have concurrent renal disease
OR stress-induced false reading - VERY COMMON
Why is hypertension important
- Risk or organs with small capillary beds
- Eye -> haemorrhage, chorioretinopathy, detachment
- Heart -> hypertrophy, murmur, arrhythmia, gallop
- Brain -> HT-encephalopathy
- Kidneys -> progressive renal disease
- -> possible catastrophic pathology before diagnosis
○ Retinal detachment
○ Why recommend older cats get annual blood pressure checks
Measuring blood pressure what is the 2 main ways and the gold standard
- Direct - gold standard
- Indirect
○ Doppler and sphygmamometer
§ Best for cats
○ Oscillometry
Good for High definition oscillmetry for dogs
Doppler measurement of BP what does it measure, cuff width needed and technique
measures systolic BP
- Cuff width = 30-40% of circumference
- Standardise protocol (white coat effect)
1. quiet environment
2. Acclimatisation period
3. At least 3-5 consistent measurements
4. Repeat abnormal findings (ensure persistent)
Approach to diagnose before there is an issue with hypertension
- Establish if possible that there is a true reading
- Full CBC, biochemistry, electrolytes
- Total T4
- Urine (cystocentesis)
- Consider abdominal ultrasound if hypokalaemia
Treatment of hypertension in cats what are the 6 main component
- Identify and treat underlying cause if possible
- Weight reduction
- Decrease dietary NaCl
- Supplement potassium if low
- Consider aldosterone antagonism if hypokalaemia (spirolactone)
- Specific hypotensive drugs
○ Amlodipine +/- ACE inhibitor
Amlodipine what is it, what does it do, onset, duration, efficacy and dosing
treatment of hypertension in cats and dogs
- Block Ca2+ influx into vascular smooth muscle -> VASODILATION
- Slow onset of action
- Long duration of action
- Good efficacy
- ONCE daily dosing
ACE inhibitors what used for, types, mechanism of action, efficacy
treatmetn of hypertension in cats and dogs
- Benazepril, enalapril, ramipril
- RAAS inhibition and weak vasodilation
- Poor efficiacy - 50% cats
- Target organ protective? Not if azotaemia
Treatment of hypertension in dogs
- Prazosin if renal failure
- Amlodipine
- ACE inhibitors minimal effect
- Beta-blockers may be considered
- Treat underlying disease
Radiographs and the brain how sensitive and pros and cons
Radiographs are insensitive for most brain diseases
PROS
- Readily available to most veterinarians
- Good screening tool for some diseases
CONS
- Limited to detecting bone changes
- Complex anatomy makes interpretation difficult
Ultrasound and imaging the brain how can work
Ultrasound doesn’t work properly -> encased in the brain which doesn’t work with ultrasound
- Thin spot (open fontanelle) in the skull -> can use to ultrasound the brain - very cranial part of the brain
- Sometimes gain access through foramen magnum
CT vs MRI what good for
CT - allows brain case to be easily seen -> skull fracture
MRI - provides the best evaluation of neural tissue - BEST FOR BRAIN - great contrast - lesions look white
CT or MRI for the following situations 1. head trauma, 2. seizures, 3 hilt tilt 4. altered mentation 5. pituitary disease 6. trigeminal or facial neuopathy
- CT - bone lesion and hameeorhage most common
- MRI - lesion looking for within brain
- CT - if peripheral (history of otitis), MRI if central
- MRI - subtle disease
- CT - most seen n CT only MRI if subtle
- MRI
Contrast studies with the brain how used, how works and examples of contrast agents
Lesions are often better seen with intravenous contrast
- Where possible always give intravenous contrast
- Contrast enhancement occurs due to increased vascularity OR breakdown of the blood brain barrier - EXAM - leak of contrast
1) Iodinated contrast agents for computed tomography
- Eg Iohexol
○ High atomic number absorbs more x-rays appears white
2) Paramagnetic contrast agents for magnetic resonance imaging
- Eg gadolinium
○ Alters the local magnetic field shortens TI relaxation time appears white on TI weighted sequence
§ HAS TO BE TI WEIGHTED
What are some important interpretation that need to occurs when imaging the brain
- Location: ○ cranial vs caudal fossa ○ lobes? brain stem? ○ intra-axial or extra-axial - Mass effect: ○ midline shift & herniation - Cerebral oedema: ○ vasogenic, cytotoxic, periventricular - Haemorrhage: how old is the lesion?
Brain anatomy for imaging what are important aspects
- cribriform plate - nasal issues may infiltrate brain through this - see if intact
- cranial fossa - everything cranial to fossis tentorium
- Brain anatomy why important?
- To correlate lesion location with clinical signs
§ DO THEY MATCH?
