Small animals resp/cardio Flashcards
Where are mechanoreceptors, chemoreceptors and cough receptors found in the airways?
Mechanoreceptors - larger airways
Chemoreceptors - medium airways
Cough receptors most numerous in larynx > trachea > bifurcation > bronchi
No cough receptors in bronchioles or alveoli
Differential diagnosis of coughing?
Compression of mainstem lobar bronchi - Left atrial enlargement - Tracheobronchial / Bronchial Lymph node enlargement - Neoplasia Stimulation of cough receptors - Laryngeal disorders - Tracheal disorders - Bronchial disorders Excessive mucus / fluid / inflammation (usually soft / moist / ineffectual cough) - Pneumonia - Bronchopneumonia - Pulmonary oedema
How to differentiate between a cough caused by cardiac or respiratory disease?
HR - normal or inc if cardiac, normal or dec if resp
Heart rhythm - regular sinus rhythm, sinus tachycardia or arrhythmias if cardiac, sinus arrhythmia if resp
When - mainly night/when resting/sleeping if cardiac, mainly on excitement/exertion if resp
Usually heart murmur if cardiac
Diastolic gallops possible if cardiac
What is involved in chronic bronchitis?
Excessive mucus production Increased goblet cell numbers Hyperplasia of submucosal glands Damage to cilia Loss of ciliated epithelium Squamous metaplasia of mucosa Secondary infections common
Aetiology of chronic bronchitis?
Unknown
Environmental factors e.g. smoking household
Previous infection
Clinical presentation of chronic bronchitis?
Typically small breed/toy breed dogs
Chronic cough with attempts at production
Worse on excitement
Prognosis guarded since most mucosal changes are not reversible
Therapeutic goal is to manage the condition
Investigations indicated in suspected chronic bronchitis case?
Thoracic radiographs
Haematology
Bronchoscopy
BAL to obtain samples for cytology/bacteriology/parasitology
Which respiratory parasites should be ruled out before diagnosing chronic bronchitis?
Oslerus osleri
Crenosoma vulpis (fox lung worm)
Aelurostrongylus abstrusus (cats)
Troglostrongylus (emerging parasite in cats - Italy/Spain)
Clinical signs of Oslerus osleri infection? Transmission?
Cough and respiratory noise
Produce nodules at the carina
No intermediate host required
Direct transmission dog-dog, bitch to pups (in resp excretions, regurgitant feeding, or via faeces in dirty environment)
Crenosoma vulpis infestation - transmission? Diagnosis?
Fox lung worm
Intermediate host requires - slugs/snails
Worms readily seen on tracheobronchoscopy (4-16mm long)
How to do BAL?
Lavage volume about 0.5ml/kg
2ml saline for BAL for cats and small dogs
10ml in large dogs (about 2-3 washed)
Should be able to aspirate about 50% of fluid
What is normal on BAL fluid (BALF) cytology?
Ciliated columnar epithelial cells Goblet cells Normal total WBC < 5 x 10^9/l Macropahges ~70% Neutrophils ~20% Lymphocytes ~10% Eusinophils <20-25%
What is usually seen on BALF cytology in chronic bronchitis?
Increased mucus
Increased neutrophils and macrophages
Possibly squamous metaplasia of normal ciliated columnar epithelial cells
Presence of bacteria/particulate matter
What is usually found on BALF bacteriological culture in chronic bronchitis?
Normally negative (aerobic and microaerophilic)
Management of chronic bronchitis?
Weight control
Harness
Avoid irritants/smoking environment
Avoid very dry environments/use nebuliser/spend time in bathroom during owner’s shower/bath (mucus easier to shift if hydrated)
Treatment drugs used for chronic bronchitis?
Bronchodilators - Theophylline, Terbutaline, Etamiphylline camsilate
Steroids
Mucolytics may be beneficial if mucociliary clearance is compromised - Bromhexine
What do bronchodilators do to help chronic bronchitis?
Reduce spasm of lower airways
Reduce intra-thoracic pressures
Reduce tendency of larger airways to collapse
Improve diaphragmatic function
Improves muco-ciliary clearance
Inhibit mast cell degranulation (reduced release of mediators of bronchoconstriction)
Prevent microvascular leakage
What do glucocorticoids do to help chronic bronchitis?
Broncho-dilatory Anti-inflammatory Inhibit both prostaglandin & leukotriene synthesis Potentiate beta-2 adrenergic activity Reduce leukocyte accumulation Induce lymphopenia & eosinopenia Reverse increased vascular permeability Alter macrophage function Inhibit fibroblast growth Modulate the immune system
Does chronic bronchitis need antibiotics?
Most cases don’t have bacterial infection as a causal agent
Secondary infection is possible
So indicated if C+S results +ve, or if intracellular bacteria seen on BALF cytology
What to consider when using antibiotics for respiratory tract infections?
Select based on C&S results if possible
Needs to concentrate in the lung
Needs to be effective against resp. pathogens
Ideally, should be bacteriocidal
May need to select combination A/B
- e.g. severe pneumonia
Need to treat for long enough (2 weeks min.)
Secondary respiratory tract infections possible
e.g. in chronic bronchitis, due to compromised mucociliary clearance
Which antibiotics are used fo respiratory infections and what are they effective against?
Clavulonate potentiated amoxycillin - broad spectrum
Fluoroquinolones - broad spectrum
TMP sulphonamides - broad spectrum, Pneumocystosis
Cephalexin: mainly effective against G-ve
Clindamycin - mainly used for G+ve (and anaerobes)
Doxycycline - if confirmed or suspected Mycoplasma or Bordetella
Metronidazole - anaerobic, some bronchopneumonias
What is four-quadrant antibiotic treatment?
For life threatening pneumonia/bronchopneumonia
Combination Abs - e.g. potentiated amoxicillin, fluoroquinolone, metronidazole
What is Eosinophilic Bronchopneumopathy (EBP) aka Pulmonary Infiltrate with Eosinophils (PIE)?
Form of chronic bronchitis with pulmonary granulomatous disease
Usually mixture of bronchial and interstitial pulmonary involvement
Usually young dogs, large breeds
Presumed hypersensitivity to inhaled allergens (or parasites e.g. migrating Toxocara canis)
What is seen on bronchoscopy and BALF cytology with Eosinophilic Bronchopneumopathy (EBP) ?
Bronchoscopy - typically copious amounts of yellow-green mucus
BALF cytology - >25% eusinophils
Treatment of Eosinophilic Bronchopneumopathy (EBP) ?
Prednisolone - immunosuppressive dose usually required, taper doses once clinical signs controlled, aim for alternate day
Could also consider azothioprine
Also possibly:
- wormer to exclude parasitic cause (fenbendazole to address migrating L3s)
- antibiotics if secondary bacterial infection (not common)
- bronchodilators esp if bronchospasm suspected
- mucolytics
What is Feline Asthma? Clinical signs?
Allergic airway disease
Reactive bronchoconstriction may also result
Present with a cough
Can have air trapping and severe dyspnoea
Expiratory dyspnoea (bronchoconstriction affects expiratory phase more than inspiratory)
May auscultate expiratory wheezes
Radiographic signs of Feline asthma?
Increased bronchial markings
Air trapping - diaphragm flattened
‘Barrel’ chested
Treatment of dyspneic cat with Feline Asthma?
Minimise stress
Provide humidified oxygen (in incubator; oxygen cage)
Give IV steroids (e.g. dexamethasone 1 mg/kg)
Bronchodilators e.g. Terbutaline (0.01 mg/kg IM or IV)
Consider MDI admin. of bronchodilators (salbutamol)
Severe, life-threatening distress: Adrenaline (0.1ml of 1:1000 IV or via ET tube)
Which drugs can be used in Metered-dose Inhalers for chronic management of feline asthma?
Salbutamol
- 1 puff bid or as required
- Effective within 5 minutes, lasts ~ 4 hours
Fluticasone
- 2 puffs bid
- Long term control of inflammation
- No systemic effects
- Takes 10 – 14 days for peak effect
Chronic management and oral treatment of feline asthma?
Keep away from environmental allergens (e.g. soft furnishings, bedrooms, carpeted rooms)
Allow outdoor access if possible - avoid very warm, dry environments
Bronchodilators - oral Terbutaline
Prednisolone - taper dose once signs controlled, aim for alternate day medication
A/B rarely indicated.
Clinical signs of bronchial foreign bodies?
Sudden onset coughing
Usually gun dog breeds (scenting/sniffing)
History of exercise through fields/arable crops/woodland
If long standing, halitosis often marked
Partial response to antibiotics
Differential diagnoses of inspiratory dyspnoea?
Laryngeal paralysis
Laryngeal neoplasia
Tracheal mass/stenosis
Differential diagnoses of expiratory dyspnoea?
Dynamic airway collapse
Feline asthma
Differential diagnoses of both inspiratory and expiratory dyspnoea?
Pulmonary parenchymal disease - pneumonia, pulmonary oedema, idiopathic pulmonary fibrosis IPF
Pleural effusions
Pneumothorax
Pulmonary thromboembolism
What is the difference between obstructive and restrictive dyspnoea?
Obstructive - tends to have a noise associated
- Inspiratory: upper airway obstruction
- Expiratory: bronchial narrowing
Restrictive - pulmonary, pleural - tends to be more rapid breathing and no noise
When would a dyspneic animal with cyanosis not respond to oxygen?
R-L shunt
How to provide oxygen therapy to dyspneic animal?
Without stress!
Via cage/incubator - small animals
Face mask, nasal catheter, elizabethan collar and cling film etc
Aim for 30-50% inspired oxygen
Avoid 100% oxygen for more than short time (oxygen toxicity)
Oxygen must be humidified
Monitor response
What is aspiration pneumonia usually associated with?
Megaoesophagus
Laryngeal paralysis
After tie back surgery
What is Pneumocystis carinii? What does it cause/when is it seen? Treatment?
Yeast like fungus
Cause of pneumonia in immune compromised human patients
Cavalier King Charles puppies have immunoglobulin deficiency and may present with dyspnoea due to PC pneumonia
Only responds to TMP sulphonamides
Clinical signs of Angiostrongylus vasorum infection?
Cough Shortness of breath Hypoxaemia Exercise intolerance Can also cause coagulopathies, neurological signs etc
Diagnosis of Angiostrongylosis?
Faecal baermanns to see larvae
Rectal swab, smeared onto slide and suspended in saline for direct microscopy
Angio detect (IDEXX)
Which breeds is Idiopathic Pulmonary Fibrosis seen in? Clinical presentation?
Predominantly terrier breeds, especially WHWT
Slow, insidious progression
Inspiratory and expiratory dyspnoea, rapid, shallow breathing, can develop rectus abdominus hypertrophy and become cyanotic on minimal exertion
Characteristic “crackles” like cellophane on lung field auscultation
Become severely disabled
How does Idiopathic Pulmonary Fibrosis appear on CT?
Peri-bronco-vascular interstitial thickening
Ground glass opacity
Treatment of Idiopathic Pulmonary Fibrosis?
Symptomatic support – nothing proven to be effective
Restrict exercise and excitement
Home delivery of oxygen when distressed? (but oxygen concentrators are expensive!)
Bronchodilators ? (especially if airway collapse or concurrent chronic bronchitis)
Steroids (Prednisolone)?
Anti-fibrotics (e.g. Colchicine)?
Clinical signs of Paraquat poisoning? Prognosis?
Severe pneumotoxin
Results in severe dyspnoea (initially with minimal radiographic findings)
Initial alveolitis progresses to severe pulmonary fibrosis
Very poor / hopeless prognosis
When is Pulmonary thromboembolism (PTE) seen?
Usually secondary to an underlying systemic disease (not usually a primary cardiac disease)
- IMHA
- Protein losing conditions - esp nephropathy
- HAC
- Pancreatitis
- Sepsis
- DIC
Clinical signs and diagnosis of pulmonary thromboembolism (PTE)?
Suspect with sudden onset dyspnoea
Normally no adventitious respiratory sounds
May be loud S2 (due to associated pulmonary hypertension - delayed closure of pulmonic valve)
Radiographic findings may not be evident or are subtle (e.g. hypoluscent region of lung field)
Arterial blood gas analysis to confirm (large alveolar to arterial oxygen gradient, A-a showing significant ventilation:perfusion mismatch)
Coagulation screen to identify clot breakdown products - FDPs, D-dimers
Treatment of pulmonary thromboembolism?
Oxygen supplementation (but large V/Q (=ventilation/perfusion) mismatch)
Sedation/anxiolytics
Treat underlying disease
Anticoagulant treatment to prevent further episodes - low molecular weight heparin
Antiplatelet medication - clopidogrel, low-dose aspirin
Clinical signs, causes and diagnosis of Acute Respiratory Distress Syndrome (ARDS)?
A form of non-cardiogenic pulmonary oedema
Respiratory distress with alveolar infiltrates on radiographs
Initiating factors - pneumonia, electrocution, smoke inhalation, near drowning, trauma, sepsis, DIC
Specific histopathological criteria for diagnosis
Causes of pleural effusions?
Increased hydrostatic pressure
Decreased plasma oncotic pressure
Increased vascular or pleural permeability (e.g. inflammation).
Increased fluid production (e.g. infection)
Lymphatic capacity can increase 30x if required
Diagnosis of pleural effusions?
Radiography - may excessively stress
Ultrasound - v sensitive at detecting fluid, good as quick and doesn’t cause distress to dyspneic animal
Thotacocentesis - blind or ultrasound guided, sternal recumbency with gentle restraint receiving oxygen, 7-8th ICS, 3 way tap on one way valve
If positive tap, continue to drain (therapeutic) - life saving in severe pleural effusions
Types of pleural effusions?
Transudates Modified transudates FIP - strwe coloured Pyothorax Chylothorax Haemothorax
Possible causes of transudate and modified transudate pleural effusion
Transudate - hypoalbuminaemia
Modified transudate - right sided biventricular CHF, diaphragmatic rupture, neoplasia
Causes of haemothorax?
Trauma
Neoplasia
Coaguloapathy
Causes of a non septic inflammatory pleural effusion?
Lobe torsion
Chronic chylothrax
Neoplasia
Causes of a septic inflammatory pleural effusion?
Ruptured oesophagus
FB
Pyothorax
Fungal infection
Causes of a chylous pleural effusion?
Idiopathic CHF CrVC obstruction Trauma Lobe torsion
Analysis of pleural effusions
Transudate - low protein and cells
Modified transudate - bit more protein and cells, may be neoplastic cells
Haemothorax - blood, mesothelial cells
Non septic inflammation exudate - neutrophils, macrophages, mesothelial cells
Septic inflammation exudate - degenerate neutrophils, bacteria, macrophages, mesothelial cells
Chylothorax - TG fluid>TG plasma, small lymphocytes
Treatment of pleural effusions after thoracocentesis?
If due to pericardial effusion, need to rapidly carry out pericardiocentesis
If due to congestive heart failure, treat as CHF
If due to hypoproteinaemia, investigate and treat the underlying condition
What to do following thoracocentesis for pyothorax?
Submit material for aerobic and anaerobic and microaerophilic culture and sensitivity
Base antibiotic selection on these results
Initially, start combination antibiotics to offer broad spectrum against G+ve, -ve and aerobes, anaerobes e.g. potentiated amoxycillin, metronidazole, fluoroquinolone combo
When stable, insert chest drain(s) under GA
Daily thoracic lavage (up to 20mls/kg warmed saline)
Once lavage fluid is clear, can pull drains
Continue A/B for 2-3 months
What can chylothorax be associated with?
Trauma or mass lesions disrupting thoracic duct/ cranial vena cava
Pericardial disease
Congestive heart failure (usually RHF, especially cats)
Lung lobe torsions
Spontaneous/idiopathic - e.g. Afghans, Bull mastiffs, oriental breeds of cats
Treatment of chylothorax following thoracocentesis?
Treat underlying cause
Feed low fat diet, high CHO (reduces chyle prod’n and alters character)
Add medium chain triglycerides to diet ?
Rutin (20 – 50 mg/kg q. 8 hours) - may reduce chyle production)
Consider surgical management
When is needle thoracocentesis used?
For one off drainage of the pleural cavity
Used when on-going requirement for drainage not anticipated
Immediate patient stabilisation
Diagnostic and therapeutic
How to carry out needle thoracocentesis?
Sternal recumbency
Give supplemental oxygen
Clip and aseptically prepare area of skin (5-10cm2) on lower 7-8th ICS
Sterile technique
16G-20G, 1-1.5inch needle or over the needle IV cannula in dogs
Butterfly cannula usually ok in small dogs and cats
Ensure patient is adequately restrained
Analgesia and/or sedation depending on patient status
Place needle/cannula through mid to caudal ICS - in the lower third of the chest for fluid, dorsal third of the chest for pneumothorax
Intercostal vessels and nerves run caudal to ribs so
avoid these
Advance needle/cannula through chest wall, directed caudally and at an angle to pass just underneath internal surface of the ribs
Aspirate air and/or fluid - measure the volume, retain samples for analysis, plain sterile tubes for culture, EDTA tubes for cytology
Bilateral pneumothorax/pleural effusion: drainage of one side of the chest may be adequate
Take thoracic radiographs after drainage
Complications of thoracocentesis?
Iatrogenic pneumothorax - laceration of pleura overlying lungs or creation of excessive negative pressure within the pleural space causing ripping of the pleura
Laceration of heart
Laceration of major arteries
Laceration of intercostal vessels or nerve
When are thoracotomy tubes used? Which side are they placed and what size is used?
For drainage of rapidly accumulating, large volume pleural fluid/pneumothorax
Side based on clinical, radiographic and thoracic ultrasound findings
Internal diameter approx half the size of the ICS
Smaller ok depending on nature of fluid (or air)
Where is a thoracostomy tube placed?
Enters chest at 7-8th ICS
Usually midway up thorax
Patient preparation for placement of a thoracostomy tube?
Usually sedated or anaesthetised IV access Administer oxygen Patient position - sternal or lateral Clip from caudal border of scapula to behind last rib Surgically prep and drape patient
Local anaesthetic for thoracostomy tube placement?
Poss more painful than needle itself?
Intercostal nerve block
Infiltrate along proposed tunnel
What must be done post thoracostomy tube placement?
Empty the pleural cavity - improves oxygenation
Radiograph thorax - check tube location, may see pathology not seen when fluid present
Post-op care of thoracostomy tube placement?
Bandage - maintain sterility, prevents patient interference
Analgesia
Close patient observation
Methods of drainage with a thoracostomy tube?
Intermittent manual - 3 way tap and syringe
Continuous - heimlich valve, underwater seal
Possible complications of thoracostomy tubes?
Damage to intrathoracic structures Air leakage through/around tube - subcut emphysema/pneumothorax Introduction of infection - pyothorax Stimulation of pleural effusion Pain Ineffective drainage Phrenic nerve irritation Arrhyhthmias
Methods to reduce complications of thoracostomy tube?
Aseptic technique Keep close to cranial edge of rib to avoid neurovascular bundles Use 7-8th intercostal space Create subcutaneous tunnel Pre-measure length required Secure tube in place Ensure connections are secure Ensure correct positioning/patency Reduce patient interference
When should thoracostomy tubes be removed? How?
ASAP
Generally when no/minimal air aspirated/<2ml fluid/kg/day
Remove on expiration
Dress skin wound, antibiotic ointment and light dressing for 24h
Drain will cause pleural fluid production of approximately 2-3ml/kg/day
Indications, advantages and disadvantages of median sternotomy for thoracic access?
Exploatory surgery - e.g. pneumothorax/pyothorac of unknown aetiology, removal of cranial mediastinal masses
Adv - gives access to both sides of thorax
Disadvs - poor access to dorsal lung field, thoracic duct and great vessels
Indications, advantages and disadvantages of intercostal thoracostomy for thoracic access?
Thoracic surgery of right OR left thorax
Adv - good access immediately adjacent to incision
Disadv - poor access to structures away from incision
Which side of the thorax would you do an intercostal thoracostomy for the heart, PDA, PRAA, cranial lung lobe, middle lung lobe, caudal lung lobe, cranial oesophagus, caudal oesophagus, cranial vena cava, caudal vena cava?
Heart - left or right PDA - left PRAA - left Cranial lung lobe - left or right Middle lung lobe - right Caudal lung lobe - left or right Cranial oesophagus - left Caudal oesophagus - left or right Cranial vena cava - (left) or right Caudal vena cava - (left) or right
Indications for lung lobectomy?
Lung lobe torsion
Localised pulmonary abscess/cyst/bullae/solitary neoplasia
Severe lung trauma
Broncho-oesophageal fistula
Initial assessment of an animal with thoracic trauma?
Maintain a patent airway - provide oxygen
Support circulation
Control obvious haemorrhage
Indications for Tube Thoracostomy?
Thoracotomy post-op management
Continued/ongoing pneumothorax despite repeated needle thoracocentesis
Severe/large volume pleural effusion - pus, malignant, chyle, sero(sanguinous?)
Treatment for rib fractures?
Conservative management usually adequate
Analgesia, rest, oxygen supplementation
What is Flail Chest?
Segment of one or more ribs is fractured in two planes
The segment can move independently from chest wall
Paradoxical movement compromises respiration
What happens with diaphragmatic ruptures?
Consequence of blunt abdominal trauma
Tear in muscular part +/- tendinous portion
Abdominal organs enter pleural space
Physical compression of lungs
Incarceration of abdominal organs can cause effusion
Best method of diagnosis of diaphragmatic rupture?
Ultrasound
What is paradoxical respiration?
Diaphragm acting in opposite way to normal
E.g. when breathing in chest moves out but diaphragm moves up
What is high rise syndrome?
Fall from >2 stories
Thoracic injuries - pneumothorax or contusions
Fractured mandible, evulsion of chin, haemorrhage in nasal cavity (land on feet/chin then sternum), bilateral distal ulna fractures
The higher cats fall, the more likely to survive as relax when reach terminal velocity and land on feet (dogs panic and land on back)
Other names for Myxomatous degenerative valve disease?
Myxomatous degenerative valvular disease (MDVD) Myxomatous mitral valve disease (MMVD) Degenerative valvular heart disease Mitral endocardiosis Chronic valvular insufficiency
Causes of valvular leaks?
MDVD
Mitral dysplasia
Mitral regurgitation in DCM
Endocarditis
What is Myxomatous degenerative valve disease?
Nodular thickening of valve leaflets - glycosaminoglycan and proteoglycan accumulation
Lengthened or ruptured chordae
Idiopathic - poss collagen and ECM formation abnormalities or abnormalities of serotonin signalling or mechanical stress
Suspected genetic basis - predisposition in CKCS
What pathology is seen with Myxomatous degenerative valve disease?
LA dilatation LV dilatation Elongation of chordal tendinae Thickened leaflets Jet lesions Arteriosclerosis in myocardium
What are the layers of the mitral valve?
Atrialis
Spongiosa
Fibrosa
Ventricularis
What happens in the heart with valvular incompetence (MDVD)?
Leakage of blood back into low pressure left atrium
Reduction in forward stroke volume
Increase in volume of blood entering left ventricle in next diastole
= Volume overload of LA and LV -> eccentric hypertrophy
Reduces after load, increases preload (increases EDV), reduces stroke volume
= Hyperdynamic systolic function
What does valvular incompetence (mitral regurgitation) (MDVD) lead to systemically?
Increased left atrial volume and increased reload -> chamber dilation and increased contractility
Reduced forward stroke volume -> activation of sympathetic NS and activations of RAAS -> increased HR and contractility, vasoconstriction (-> increased after load), increased circulating volume
What neurohumoral activation occurs as a result of valvular incompetence (MDVD) and DCM?
Sympathetic NS - tachycardia, positive inotrope, vasocontriction
RAAS - retention of Na and fluid, increased circulatory volume, vasoconstriction
Remodelling (MDVD) - myocardial hypertrophy - improved systolic function
What are the sequelae to neurohumoral activation (decompensation) as a result of valvular incompetence (MDVD) or DCM?
Sympathetic nervous system (tachycardia, vasoconstriction)
- Toxic for myocytes -> intracellular Ca overload
- Increased oxygen demand
- Cell death, decrease in systolic function
RAAS
- Increased circulatory volume
- Increased hydrostatic pressures – congestion
Romodelling (eccentric hypertrophy)
- Fibrosis (arrhythmias)
- Increased wall stress
- Dilatation of the valvular annulus -> MR
Clinical signs of MDVD?
Small breeds (but can be any) Loud heart murmur (left apical systolic) - starts quiet Dyspnoea, tachypnoea, crackles Adult dogs (inc likelihood as gets older) Collapse less likely Exercise intolerance Cough Increased respiratory rate and effort But poss no clinical signs ar all!
Diagnostics for MDVD? Why useful/what to look for?
Blood pressure - often normal - hypertension -> increased after load -> worse regurgitant fraction - hypotension if forward (systolic) failure Radiography - sedation - DV and right lateral - cardiac size - tracheal elevation, bulges, VHS - pulmonary vessels - lung infiltrate - effusions? Clinical pathology - biomarkers (NTproBNP) - helpful to differentiate resp/cardiac cause of cough - to assess severity - predict onset of CHF? - prognostic indicator - can also look at electrolytes, azotaemia, troponin I ECG - supra ventricular premature complexes - atrial fibrillation - ventricular premature complexes Echocardiography - confirms diagnosis - severity and progression - B lines - enlarged LA - significant mitral regurgitation - dilated, rounded LV - hyper dynamic systolic function - tricuspid regurgitation - pulmonary hypertension
How to do VHS?
Right lateral
Carina = black circle where bronchi bifurcate
Measure from carina to apex
Measure widest width
From front of T4, measure carina-apex and width lengths along the vertebrae and see how many vertebrae it is
Add the 2 numbers together
Normal LA and LV shape and LA:aorta?
LA - square
LV - bullet shape
LA 1.5 x aorta
CHF treatment for dogs?
Standard: Furosemide, Pimobendan, ACE-inhibitor, Spironolactone
If supra ventricular arrhythmias: Diltiazem, digoxin
If ventricular arrhythmias: Sotalol
If pulmonary hypertension: Sildenafil
Nutraceuticals - omega 3 fish oils
Cough suppressants (be careful!) - codeine, butorphanol
When is pimobendan licensed for preclinical MDVD?
Evidence of grade 3 murmur or above
Evidence of cardiomegaly
- echo (inc LA/Ao and LVIDd) and radiography VHS >10.5
- no echo - murmur 3 or above and VHS 11.5 or above or an increase in VHS of 0.5 or more in 6 months
Prolongs preclinical phase by 462 days
60% extension in symptom free survival
Prognostic predictors used for MDVD?
Left ventricular dimensions
Left atrial enlargement
Rupture of major chorda
NT-proBNP
Prognosis of MDVD?
Very variable
Some asymptotic dogs never develop CHF
CKCS better prognosis (earlier onset)
Once CHF signs appear, prognosis worse but variable timeline
Large breed dogs can show myocardial failure and deteriorate more rapidly
Which bacteria can cause endocarditis? Which valves affected most?
Streptococcus Staphylococcus E.coli Pseudomonas Bartonella etc Mitral, aortic > tricuspid, pulmonic (in small animals)
Requirements for endocarditis?
Bacteriaemia (infection, IV catheter, surgery)
Damaged endothelium (turbulence, high velocities)
Ability to adhere
Hypercoagulable
states
What pathology is seen with endocarditis?
Vegetations of endocardial surface of leaflets - small nodules, polypoid Perforated, deformed, calcified Microscopic findings: - platelets, RBC, WBC, bacteria, fibrin - fibrous tissue, calcification - bacteria within vegetations
Diagnosis of endocarditis?
Haematology, biochemistry CTnI BLOOD CULTURE - Prior to antibiotics - Aseptic techniques - At least 3 puncture sites, 10 ml per sample, change needles when injecting into bottle - Frequently false negative, can be false positive (skin contamination) ECHOCARDIOGRAPHY - Valvular vegetations - Size -> risk embolisation - Regurgitation = MURMUR! - Systolic dysfunction
Modified Duke’s criteria for endocarditis?
Major criteria:
- Positive echocardiogram - vegetative, oscillating lesion, erosive lesion, abscess
- New valvular insufficiency
- Positive blood culture - ≥2 positive cultures, ≥3 positive cultures with skin contaminant
Minor criteria:
- Fever
- Medium/large breed
- Subaortic stenosis
- Thromboembolic disease
- Immune-mediated disease - polyarthritis, glomerulonephritis
- Positive blood culture not meeting major criteria
- Bartonella serology ≥1:1024
Treatment for endocarditis?
Aggressive antibiotics (or poor prognosis)
- bactericidal (based on sensitivity)
- combination
- IV initally
- minimum 6 weeks - CRP for long term follow up?
- anticoagulation - clopidogrel, aspirin
Plus if go into CHF
Prognosis of endocarditis?
Guarded
Recurrence and complications possible
Long term valvular damage
What is a cardiomyopathy?
Myocardial disorder in which the heart muscle is structurally and functionally abnormal
What primary cardiomyopathies are there?
Dilated cardiomyopathy (DCM) - most common
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
Hypertrophic cardiomyopathy (HCM)
Atrial cardiomyopathy
What secondary causes of cardiomyopathies are there?
Tachycardia induced Hypertensive Drugs/Toxins Infiltrative Metabolic/endocrine Nutritional - taurine, L-Carnitine Inflammatory (myocarditis) - infectious, non-infectious Connective tissue disease - muscular dystrophy (GR, GSD)
How does the heart present with DCM?
Impaired systolic function
Dilated cardiac chambers (L>R, HW:BW increased, thickness LV:diameter LV decreased (thin walls)
Mitral/tricuspid annulus stretched
Heart markedly enlarged
Which 3 key breeds are affected by DCM?
Dobermann
Newfoundland
Great Danes
Aetiology of DCM?
Idiopathic
Probably genetic components
Histopathology of DCM?
Attenuated fibers (atrophied) - myocytes thin, degeneration, fibrosis Fibro-fatty infiltration - myocyte lysis, vacuolation, fibrosis, fatty infiltration, boxers with ARVC
What are the sequelae to DCM pathology?
Damaged cells no longer function effectively as a syncytium
Cell death and fatty or fibrous replacement
-> IMPAIRED SYSTOLIC FUNCTION
-> reduced CO -> activation of sympathetic NS and RAAS -> increased HR and contractility, myocardial hypertrophy -> increased myocardial oxygen demand, increased wall stress, CO and BP maintained -> further myocardial cell death, myocardial fibrosis -> impaired systolic function
Similarities and differences between MDVD and DCM?
Similarities:
- Enlargement of left ventricle (+/- right)
- Enlargement of left atrium
- Mitral regurgitation
Differences:
- MDVS lots of mitral regurgitation, DCM mild mitral regurgitation
- MDVD normal/hyperdnamic systolic function, DCM reduced systolic function
- MDVD LA>LV, DCM LV>LA
Clinical presentation of DCM in Dobermanns?
High prevalence (approx. 60%) Slowly progressive, inherited Long asymptomatic preclinical phase Ventricular arrhythmias (♀) Sudden death Cardiomegaly less obvious Annual screening, short survival after CHF
Clinical presentation of DCM in Great Danes?
High prevalence?
Frequent VPCs, atrial fibrillation
Sudden death
Clinical presentation of DCM in Irish wolfhounds, cocker spaniels, dalmatians and portuguese water dogs?
Irish Wolfhounds - ‘lone’ atrial fibrillation -> progression to overt DCM?
Cocker spaniesl - ‘benign’ slow progression over years, taurine!
Dalmatians - VPCs, low protein?
Portuguese water dogs - juvenile onset (<1yr), highly aggressive, poor prognosis
Histopathology of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?
Loss of myocytes with fatty/fibrofatty replacement
Presentation of Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?
- Asymptomatic with VPCs
- Symptomatic with VPCs
- Ventricular dilation, myocardial dysfunction, arrhythmias
Ventricular arrhythmias (> 91 VPCs/24h; >1000 VPCs/24h)
Asymptomatic, sudden death, progress into CHF
Adult-onset, inherited
Syncope, exercise intolerance
Most common in Boxers - inc chance of sudden death, poss genetic involvement
Atrial cardiomyopathy?
English Springers and Labradors
Hugely enlarged left atrium with thin walls
Atrial standstill - bradycardia with no P waves (need pacemaker)
Hypertrophic cardiomyopathy?
Rare, similar to feline HCM – usually HOCM
Terrier breeds, Pointer dogs, Golden Retriever
Remember exclusions!
Which breeds can get secondary cardiomyopathies due to taurine deficiency? Diagnosis and treatment?
Proven in American Cocker Spaniels and known to be present in English Cocker Spaniels
Supplementation leads to improved systolic function (but may not ’cure’ the disease)
Measure taurine in any DCM-like case of a non-typical breed
Clinical signs of cardiomyopathies?
Larger breeds Arrhythmia Quiet, soft heart murmur, left apical systolic Dyspnoea, tachypnoea, crackles Adult dogs, increased likelihood as dog gets older Collapse quite common Exercise intolerance Cough Increased respiratory rate and effort Possibly no clinical signs at all! Sudden death risk!
Diagnosis of cardiomyopathies?
History + physical examination
Blood pressure
- Systolic hypotension (low if forward failure – systolic dysfunction)
- Systolic hypertension (Increased afterload → increased myocardial oxygen demand and workload → increased risk of arrhythmia →increased mitral regurgitant fraction)
Clinical pathology - biomarkers (azotaemia, electrolytes, thyroid, NT-proBNP, troponin I), genetic testing (PDK4, Striatin)
ECG
Radiography - DV and right lateral, cardiac size (tracheal elevation, bulges), pulmonary vessels, lung infiltrate, effusions
Echocardiography
Ambulatory ECG
What may be seen with MDVD and DCM on ECG?
SVPCs
VPCs
Atrial fibrillation
DCM only - ventricular tachycardia
Comparison of MDVD and DCM on echocardiography?
MDVD: - Enlarged left ventricle and atrium but LA>LV - Dilated left ventricle - Rounded left ventricle - Hyperdynamic systolic function - Lots of MR DCM: - Enlarged left ventricle and atrium but LV>LA - Dilated left ventricle - Rounded left ventricle - Thin walls - Reduced systolic function - Mild/moderate MR
Holter - ambulatory ECG?
Use for: - Screening for DCM/ARVC - Arrhythmia identified on physical exam - History of collapse VPC numbers: - Normal dogs: < 4/24h, 0-50 single VPCs - Indeterminate: 51-100 - Suspicious: doberman > 50, boxer 100-300 - Likely affected: 300-1000 - Affected > 1000
Treatment for preclinical DCM?
Pimobendan!
PROTECT study in Dobermanns
Prolongs time to onset of CHF or sudden death
9 months additional clinical symptom free time
And pose ACE-I - retrospective study in Dobermanns
Prognosis of DCM?
Very variable
in general guarded-poor, depending on response to treatment - monitoring important
6-12m (less in certain breeds)
Dobermann 2-4 years preclinical phase then 4-6 months once in CHF
Boxer with ARVC lifespan apprx 11 years but increased sudden death
American Cocker Spaniels with Taurine deficiency better - improvement after supplementation of Taurine
English Cocker Spaniels > 2y after onset of CHF
Negative prognostic indicators:
- Young age
- Ascites
- Dyspnoea
- Atrial fibrillation
What feline primary myocardial diseases are there?
Hypertrophic cardiomyopathy (HCM) Hypertrophic (obstructive) cardiomyopathy
(HOCM)
Unclassified cardiomyopathy (UCM)
Restrictive cardiomyopathy (RCM)
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
Dilated cardiomyopathy (DCM)
What feline secondary myocardial diseases are there?
Hypertensive cardiomyopathy Hyperthyroid cardiomyopathy Cardiomyopathy associated with: • acromegaly • azotaemia • diabetes mellitus
Clinical signs of feline cardiomyopathy?
May be asymptomatic (preclinical)
- murmur (doesn’t correlate well with disease)
- arrhythmia e.g. VPCs
- gallop sounds
Left sided CHFF - acute presentation with life threatening pulmonary oedema
Right sided CHF - ARVC especially
(Aortic) Thromboembolism
Sources of murmurs in H(O)CM?
Septal bulge (hypertrophy) results in LVOT (LV outflow tract) obstruction Systolic anterior motion of MV (SAM)
What are S3 and S4?
S3 = rapid deceleration of blood in LV S4 = LV filling associated with atrial contraction
Signs of thromboembolism in cats?
Terminal aorta (saddle thrombus) - bilateral paralysis of hindlimb (cold) Black paw pads
What is important to do with feline systemic hypertension?
Screen for underlying systemic disease - haematology, biochem, TT4
Evaluate for secondary cardiomyopathy
Recognise before CNS/ocular signs develop (retinal detachment)
Screening for Feline Cardiomyopathy?
HCM common (>25% of felines)
Pedigree breeding cats screened annually by echo
Echo main method of diagnosis but expensive, time consuming and requires vet expertise
NT pro-BNP SNAP test - immediate results so v useful in dyspneic patient to identify/exclude cardiac disease, not useful to screen healthy cats for HCM as need very high values to be abnormal on test
Where is BNP from?
Left ventricle when it becomes dilated
What pathology of the heart is seen with Feline HCM?
Marked LV concentric hypertrophy (>6mm thickness) Thickened papillary muscles Fibrosis Diastolic dysfunction Histopath: cardiomyocyte fibre disarray
What must be excluded to diagnose Feline HCM?
Systemic hypertension Hyperthyroidism Chronic renal failure Acromegaly (+/- diabetes mellitus) Aortic stenosis
Cause of feline HCM?
Familial disease reported in Persians, Ragdolls, Maine Coons, American shorthairs etc
Autosomal dominant trait
Maine coon and Ragdoll - mutations detected in Myosin binding protein C
Echocardiography for Feline HCM?
Start to worry when LA enlargement on echo - use LA:Ao
Biphasic acceleration - ‘scimitar shaped’ aortic outflow
Green on colour echo = turbulence
Thickened walls and papillary muscles (bright white = fibrosis)
Feline HCM on radiography?
Big cardiac silhouette - >2 rib spaces wide (lateral view)
‘Valentine’ heart - on DV, sign of dilated LA and/or RA
Pulmonary oedema - mottled lungs
What may be seen with ECGs for Feline HCM?
May be unremarkable
Will confirm the presence of arrhythmias and diagnose the arrhythmia
May show LV enlargement with tall R waves (>0.9 mV)
Frequently show intraventricular conduction disturbances e.g. Left anterior fascicular block (LAFB)
Diagnostic methods of Feline HCM?
Echocardiography Radiography ECG Blood pressure - always! Haematology, biochemistry, electrolytes Total T4 if >7yo NT proBNP Cardiac troponin I
Treatment for asymptomatic Feline HCM?
No evidence
Clopidogrel if LA dilated (LA > 17mm or LA:Ao > 2)
ACE-I
Diltiazem (positive lusitrope) - no evidence for licensed prep in UK
Beta blocker (atenolol) - reduce severity of dynamic LVOT obstruction/SAM, slow HR, improve diastolic function, never use in cat with uncontrolled CHF!
What are the 2 forms of feline restrictive cardiomyopathy and what are they characterised by?
Myocardial and endomyocardial forms Relatively normal LV wall measurements Relatively normal LV chamber dimensions Relatively normal LV systolic function Usually marked LA enlargement Diastolic function: restrictive physiology
What is seen with restrictive cardiomyopathy on echocardiography?
Myocardial form: ‘Smoke’ in LA = blood stasis in LA
Endomyocordial form: weird LV shape, bright white fibrosis
What happens with Arrhthmogenic RV cardiomyopathy in cats?
Fatty replacement of myocardium, initially around RRVOT
(Supra)ventricular arrhythmias or conduction disturbances
R-CHF
When is DCM seen in cats?
Rare
Taurine deficiency - assess response to taurine supplementation
Treatment of feline DCM?
Warmth (not heat mats) Oxygen Drain significant pleural effusions Furosemide IV Pimobendan e.g. 0.625 or 1.25 mg BID PO or 0.15mg/kg IV (unlicensed for cats) Other positive inotropic support e.g IV dobutamine (B1 agonist) ACE inhibitors (care BP) Taurine 250 mg tablet bid
Treatment of CHF in cats?
Furosemide
ACE inhibitor (Benazepril) – Only if BP normal
+/- Spironolactone
+/- Clopidogrel/ aspirin
+/- Potassium supplementation
Other drugs as indicated e.g. pimobendan (NOT HOCM)
Treatment of a dyspneic cat?
These cats are very fragile
DO NOT STRESS!
Provide oxygen without additional stress (oxygen cage in quiet, dark room)
FAST scan for pleural effusion/size of LA
Thoracocentesis if pleural effusion - samples for cytology +/- culture
Administer furosemide (IV if catheter can be placed without stress; otherwise IM or SC)
Sedation if very anxious (opiates e.g. methadone)
Diagnostic tests only once stabilised
Layers of the pericardium?
Outer - fibrous
Inner - serous
- Parietal layer
- Visceral layer - epicardium
Function of the pericardium?
Pericardial fluid – 0.25 mL/kg lubricant Prevents over dilation Systolic function (torsion) Co-ordinates LV-RV interaction Protects heart Maintains position But is not a vital organ
What congenital and acquired pericardial diseases are there?
Congenital - PPDH, pericardial cyst, pericardial defect/absence
Acquired - pericardial effusions, contractive/effusive-constrictive pericarditis
What are the most common causes of pericardial effusions in dogs and cats?
Dogs - idiopathic (St Bernard, GR, Labrador), neoplasia (haemangiosarcomas, chemodectoma, mesothelioma etc)
Cats - CHF (FIP)
Exclusions diagnosis for idiopathic pericardial effusions in dogs?
No mass on echo
Cytology negative for neoplasia
Occult neoplasia?
Mesothelioma?
Where may haemangiosarcomas be seen in dogs? Which dogs more prone? Treatment?
GSD, GR, Setters Right atrium, spleen, liver Quick recurrence of PE Grave prognosis Palliative treatment Pericardiocentesis Pericardectomy Balloon pericardiotomy Chemotherapy +/- surgery
Other names for chemodectoma? Breeds prone? Behaviour?
Other names - aortic body tumour, heart base tumour Brachycephalic breeds - chronic hypoxia? Slow-growing BENIGN Locally invasive Low metastatic rate Treatment - palliative pericardiectomy
Diagnosis and treatment of mesotheliomas? Causes?
No breed predisposition Chronic inflammation? Asbestos exposure? DIFFICULT TO DIAGNOSE!! - Cytology and biopsy difficult! - IHC - new panels of markers Multicavitary effusions Treatment - palliative, chemotherapy POOR PROGNOSIS
Impact of pericardial effusions?
Accumulation of fluid in pericardial sac -> reduced right ventricular filling
- > Reduced SV -> reduced left ventricular filling -> reduced LV SV -> weak pulses, collapse, tachycardia, RAAS activation -> R-CHF, ascites, pleural effusions
- > Reduced venous return to left side -> R-CHF, ascites, pleural effusions
- > During inspiration RV fills better -> ventricular interdependence -> further reduction of LV filling during inspiration -> pulses paradoxus
When does cardiac tamponade happen with pericardial effusions? What happens?
Intrapericardial pressure > RA (RV) pressure
RA collapses during diastole
Cardiac filling is severely impaired
Results in R-CHF
Clinical signs of pericardial effusions in dogs (and cats)?
Non specific signs: - Decreased appetite - Lethargy - Gastrointestinal upset Specific signs: - Abdominal enlargement - Decreased exercise tolerance - Mild coughing - Syncope/collapse NB cats are likely to present in CHF
Clinical signs of chronic pericardial effusions in dogs?
R-CHF - Abdominal effusion - Postive hepatojugular reflux - Jugular distension/pulsation - Tachycardia Femoral pulses - Weak - Pulsus paradoxus Muffled heart sounds
Clinical signs of acute pericardial effusions (usually haemangiosarcoma) in dogs?
Weak Collapsed Tachycardic Pale MM Arrhythmic potentially Signs of haemorrhagic shock Signs of forward failure Weak pulses
Diagnostic procedures for pericardial effusions?
PCV! Haem, biochem, CTnI (BEFORE pericardiocentesis) Coags BP ECG - Small QRS, sinus tachycardia, Electrical alternans (alternating QRS size) confirms PE as heart swinging in effusion Echocardiography Radiography Abdominal ultrasound FLUID ANALYSIS
How does a pericardial effusion appear on radiography?
Distinct cardiac silhouette
Cardiomegaly
Lobar pulmonary vessels small (normal)
Fat caudal vena cava
Treatment for pericardial effusions in dogs and cats?
DO NOT use Furosemide in dogs with PE
Can use Furosemide in cats as often from CHF
IV fluids in dogs (if haemodynamically unstable)
Not fluids in cats if secondary to CHF
Periocardiocentesis with cardiac tamponade in dogs
But treat the CHF in cats (if present and usually is) not pericardiocentesis
How to do pericardiocentesis?
Check patient PCV Mild sedation - opiates ideal Left lateral recumbency Right lateral access 5th -6th ICS - avoid coronary artery, window (no lungs) Prepare area 3rd-8th ICS Echo - check incision point Local anaesthetic - skin & pleura, 2% lidocaine 14G over the needle catheter 3 way tap ECG Fluid analysis
Pericardial fluid analysis?
Measure amount
EDTA tube:
- PCV - perform quickly and compare to patient PCV in case of haemorrhage
- Cytology - reactive mesothelial cells, RBC, phagocytic cells, bacteria, neoplastic cells
Plain:
- Check for coagulation (will clot if from heart)
- Culture
What should happen during periocardiocentesis?
Improvement of cardiovascular parameters:
- Reduction in HR
- Improvement in pallor
- Improved pulses
- Taller QRS on ECG
If these are not improving check fluid PCV vs dog PCV as may be draining whole blood - iatrogenic cardiac puncture, bleeding cardiac neoplasia causing hemorrhagic effusion
In this case STOP draining otherwise EXSANGUINATION!
What does/may happen after periocardiocentesis and what do you need to do?
Natural diuresis (ascites will resolve) via natriuretic peptide release
Hospitalise 12-24 hours
- Atrial fibrillation
- Ventricular arrhythmias
- Weigh twice per day
If quick recurrence/not marked improvement: neoplasia = poor prognosis
What is constrictive pericarditis? Causes? Treatment?
Rare!
Thickened, fibrotic pericardium
Idiopathic or secondary to recurrent PE, neoplasia, foreign body, infectious etc
R-CHF, cardiac tamponade with little fluid
Pericardectomy, pericardial stripping
Guarded prognosis without pericardiectomy
Difficult to diagnose
Specialist Cardiology needed
What is PPDH and when is it seen?
Peritoneal-pericardial diaphragmatic hernia
Defect of closure of ventral diaphragm and pericardium - abdominal organs within pericardial sac
Weimaraners and Persian cats predisposed
Often incidental finding
May have other malformations - sternal abnormalities, ventral abdominal hernias, congenital disease (PS, VSD)
When may left atrial ruptures be seen? Treatment?
Advanced MDVD Severe LA enlargement Atrial tears If tamponade: pericardiocentesis, blood transfusion, thoracotomy Guarded prognosis
Causes of infectious pericarditis? Treatment?
Foreign body, penetrating wound, infectious agent FIP in cats Aggressive antibiosis Fluid Culture Exploratory thoracotomy Pericardiectomy
Pericardial disease prognosis?
Idiopathic may never recur - often good long term prognosis
Quick recurrence: neoplasia
If multiple recurrences: PERICARDECTOMY palliative
Haemangiosarcoma probably worst prognosis
Chemodectoma benign, slow growing
What refines congenital heart disease murmurs?
Timing of the murmur (systolic, diastolic, continuous)
Point of maximal intensity (PMI) of the murmur
Radiation of the murmur
Pulse quality
Precordial impulse
Pathophysiology of a Patent Ductus Arteriosus? Where is the murmur heard?
Shunt from descending aorta to PA
Aortic pressure > pulmonic in systole & diastole
(continuous murmur)
Continuous “run-off” of blood into pulm. circ. (femoral pulse may be “tapping” - hyperkinetic)
Pulmonary over-circulation (Radiographs: can see increased pulmonary vessel size)
Volume overload of LA & LV
Dilation of Mitral valve annulus: secondary MR
Increased LA & LV EDP results in LHF
Myocardial failure is a common consequence
Which breeds is PDA most commonly seen in?
Rare in cats, common in dogs Bitches much more commonly affected than males GSD Collies Bichon Frise Poodles CKCS Irish setter
Clinical signs of PDA? Problem if left unrecognised/untreated?
Initially may be completely asymptomatic
Continuous murmur, left axilla, may be very localised (so often missed at first puppy exam)
Murmur may radiate (esp. systolic component)
Secondary murmur (systolic) of MR
Rapidly collapsing femoral pulse
(“tapping”, “waterhammer”)
Large systolic - diastolic pulse pressure diff.
If unrecognised/untreated, CHF intervenes in most cases by 7yo
Radiographic findings of PDA?
LA and LV enlargement
“Apparent” right sided enlargement
On DV, may have pathognomic “triple knuckle”
(aortic, pulmonic and left auricular appendage
bulges)
Pulmonary over circulation (arteries and veins increased)
+/- evidence of LHF
ECG findings with PDA?
Evidence of LA and LV enlargement
P mitrale
Tall R waves (can be very tall)
May have arrhythmias e.g. atrial fibrillation
Echocardiography findings with PDA?
2D and M-mode - LAE, LVE: dilated pulmonary trunk - ‘funnel shaped’ ductus
Colour flow Doppler - continuous, waxing and waning flow through ductus
PDA treatment?
Should be corrected before CHF or myocardial failure develops
Surgery - thoracotomy, ligation of the ductus
Or catheterisation based occlusion of PDA (femoral artery/venous catheterisation)
Early diagnosis and correction of PDA means patient is CURED!
Once CHF/myocardial failure develop, much more guarded prognosis
Which breeds are most prone to (sub)aortic stenosis? Difference in dogs to cats?
Boxers, Newfoundlands, Golden Retrievers, Rottweilers, Bull Terrier
No sex predisposition
Uncommon in cats - uniformly severe, poor prognosis
All degrees of severity in dogs
Pathophysiology of aortic stenosis?
Fixed (or dynamic) obstruction at aortic valve or LVOT level
Increased afterload on LV = pressure overload
Develops concentric hypertrophy (LVH)
Increased aortic velocities
Coronary perfusion compromised (poor coronary filling and increased wall stress)
Myocardial ischaemia may result in ventricular arrhythmias
Clinical signs of aortic stenosis?
Harsh, ejection type mid to holosystolic heart murmur
Grade of heart murmur corresponds to severity of stenosis
Radiates up carotids and on right chest
Femoral pulses may be weak
Occasionally aortic regurgitation may also result in audible (diastolic) murmur - gives a ‘to-and-fro’ murmur
What may be seen with aortic stenosis on echocardiography?
Colour flow doppler: turbulence at aortic valve
Post stenotic dilation of Aorta
Sub-valvular ridge in LVOT
What is the modified Bernouilli Equation?
PG = 4V^2 PG = Pressure gradient, mmHg v = velocity, m/s
How are aortic and pulmonic stenosis severity graded?
By aortic velocity and pressure gradient Normal speed: < 1.7m/s Mild: 0-50mmHg Moderate: 50-80mmHg Severe: > 80mmHg
Treatment of aortic stenosis?
No surgical treatment is possible (would require cardiopulmonary bypass)
Cutting balloon valvuloplasty (high morbidity & mortality)
With severe LVH, clinical signs (e.g. syncope), or ventricular arrhythmias, consider BETA BLOCKERS (survival benefit not proven)
If CHF, requires diuretics etc.
AVOID positive inotropes (Pimobendan) or arteriodilators in fixed obstruction
Breeds more prone to pulmonic stenosis?
Quite common in dogs, rare in cats
Cocker spaniels, CKCS, terriers, beagle, bulldog, bullmastiff, boxer
In some ‘bull breeds’, may be associated with aberrant coronary arteries wrapping around pulmonary trunk
Clinical signs of pulmonic stenosis?
Exercise intolerance
Syncope
May be incidental heart murmur
Mid to holo-systolic murmur cranially left heart base, radiating dorsally
Grade of murmur correlates with disease severity
If severe, precordial impulse may be stronger on the right than the left hemithorax
Pathophysiology of pulmonic stenosis?
Fixed obstruction at pulmonic valve
Increased afterload on RV
Concentric RVH
Increased velocity of pulmonic outflow
If RV pressures equal/exceed LV pressures, altered IVS motion (may be paradoxical) and LV can appear “squashed”
RV hypertrophy may lead to myocardial ischaemia - ventricular arrhythmias may result
What may be seen with pulmonic stenosis on radiography?
Right ventricular enlargement
Apex tipping
Pulmonary cap
Pulmonary bulge on DV (post-stenotic dilation)
What may be seen on ECG with pulmonic stenosis?
Negative QRS in lead I
Deep S waves in leads I, II and aVF
Right axis deviation
Treatment of pulmonic stenosis?
Cardiac catheterisation approach - Balloon Valvuloplasty of valvular stenosis, good response, aim to reduce pressure gradient by 50%
Surgical approaches - techniques to dilate pulmonic annulus, indicated if significant RVH and infundibular hypertrophy
Breeds most affected by ventricular septal defects (VSD)?
One of the more common congenital defects in cats
Less common in dogs
Cocker Spaniel, WHWT
Clinical signs of VSD?
Left to right shunt LV to RV in systole
Systolic heart murmur - PMI right hemithorax, more caudally on L “diagonal murmur”
May have murmur of “relative Pulmonic
Stenosis ” (increased volume of blood out of RV through PV)
Murmur is inversely correlated with disease severity
- Small defects, maintained PG between LV and RV: very fast, turbulent flow and very loud murmur
- Large defects, increase in RV pressure: less fast turbulent flow, lower grade murmur
Pathophysiology of VSD
Left to right shunt Volume overload of RV Pulmonary overcirculation Volume overload of LA & LV Left sided heart failure may result
Sequelae to VSD?
Small, restrictive VSDs remain asymptomatic
Left sided heart failure with large defects
With growth, some VSDs may close
Aortic valve leaflets may prolapse into VSD - functionally “closed” but aortic regurgitation develops
If pulmonary hypertension is associated with the VSD, high RV pressures may result in shunt reversal (right to left) (Eisenmenger’s syndrome)
Breeds most affected by AV valve dysplasia?
One of the most common congenital defects in cats
Mitral - bull terriers, golden retrievers, great danes, GSD
Tricuspid - Labradors
Pathophysiology of AV valve dysplasia?
Incompetence of MV/TV, with MR/TR Volume overload of LA/LV or RA/RV Left / Right sided heart failure Possible arrhythmias (especially atrial e.g. supraventricular tachycardia, AF) Occasionally get STENOSIS of MV (or TV) Rarely detect a diastolic murmur (mitral inflow) Gross atrial enlargement results Severe decompensation if AF develops
What may be seen on echo with atrioventricular valve dysplasia?
Massive atrium
Hockey stick valve?
What is Tetralogy of Fallot?
Pulmonic stenosis Right ventricular hypertrophy Ventricular septal defect Dextraposed aorta (Often hypoplastic pulmonary artery)
How to differentiate between a supra ventricular and ventricular arrhythmia?
Supraventricular - QRS tall and narrow
Ventricular - wider
Which ions do nodal and ventricular originated arrhythmias depend on?
Nodal - calcium
Ventricular - sodium
What is the Vaughan Williams Classification of anti arrhythmic drugs?
Class 1: Sodium channel blockers (slow upstroke of action potential)
Class 2: B blockers
Class 3: Potassium channel blockers (delays depolarisation, lengthens action potential duration)
Class 4: Calcium channel blockers (act on nodal tissue, SAN or AVN)
Types of supraventricualr tachycardias (SVT)?
(Sinus tachycardia - normal physiological response)
Ectopic focus -> atrial tachycardia or junctional tachycardia
Re-entry circuit -> atrial fibrillation or accessory pathway
Emergency treatment of SVT?
Vagal manoevre - push on eyeballs (dogs), massage neck, stimulate nasal plant in cats
IV Esmolol (ultra short acting B blocker)
IV Diltiazem
Oral Diltiazem if no IV prep
Oral Sotalol also possible
What is the SVT: accessory pathway (Wolf-Parkinson-White Syndrome)?
Abnormal connection between atria and ventricles
Conduction to ventricles across the pathway – short PR interval
Slurred QRS upstroke called delta wave
Young dogs (e.g. Labradors) with SVT (usually 1 – 2 years old at presentation)
Can present in heart failure (tachycardia induced cardiomyopathy)
Should exclude as this may be cured with RF ablation!
What is atrial fibrillation? What does it look like on an ECG?
Associated with cardiac disease - atrial stretch in small animals
e.g. with DCM
Irregular rhythm with tall and narrow QRS and no P waves
Treatment of atrial fibrillation?
Treat underlying cardiac disease +/- CHF
Rate control vs rhythm control
In dogs - normally accept rate control (underlying disease with atrial stretch)
Goal: control ventricular response rate to AF
Use drugs which slow conduction through the AVN
- Digoxin and diltiazem combined (better control if combined, but can use diltiazem alone if toxicity concerns)
- Beta blocker (never add to uncontrolled heart failure as if poor systolic function will fail to tolerate a negative inotrope, if tried must be v low dose, but diltiazem better)
What are the effects of Digoxin? Used for? Problem with it?
Used for atrial fibrillation
Negative chronotrope (slows HR)
Weak positive inotrope (improves systolic function)
Vagomimetic (enhances vagal tone)
Potential for toxicity - start with cautious dose and check plasma levels 5-7d later, 8h post pill
How to monitor AF rate control with treatment?
1 week after starting rate control treatment:
- check digoxin levels
- gold standard: 24h Holter monitor
Aim: HR < 140bpm (ideally < 125bpm)
If financial constraints: auscultation in clinic, HR < 155bpm
When to treat ventricular tachycardia?
Look at patient!
Treat if haemodynamically significant (check mm, CRT, pulse quality etc)
Treat if rate >200bpm
Treat if multifocal (positive and negative complexes)
Treat if close coupling (R-onT phenomenon)
Aiming to prevent ventricular fibrillation -> death
Make sure no electrolyte or acid-base disturbances
Underlying causes of ventricular arrhythmias?
Cardiac disease: - CHF - myocardial hypoxia/ischaemia - cardiomyopathy e.g. DCM Non-cardiac: - abdominal disease e.g. GDV, splenic lesions - inflammatory disease e.g. sepsis, pancreatitis - neoplasia - catecholamines - acidosis - hypokalaemia - thoracic trauma (myocardial contusions) - drug induced e.g. digoxin
Treatment of ventricular tacky-arrhythmias?
Intravenous anti-arrhythmics
- Lidocaine (class 1B anti-arrhythmic)
- Esmolol (class 2 anti-arrhythmic)
- Amiodarone - care!
Oral anti-arrhythmics
- Sotalol (class 3 with some class 2, most commonly
used)
- Mexilitine (class 1B, not readily available)
- Beta blocker e.g. atenolol (risk if underlying heart disease)
- Amiodarone (class 3; effects in all classes)
Emergency treatment of ventricular tachycardia?
Be prepared for CPR
IV access
IV bolus of Lidocaine (mg/kg) while monitoring ECG
Monitor for side effects e.g. vomiting, neuro
Max dose: 8-10mg/kg
If successful, CRI 25-50 mg/kg/min
Change to oral drugs e.g. sotalol if required within 24h
If not effective:
- check for hypokalaemia, acid base disturbances, other diseases, pain
- oral medications: sotalol (takes approx. 30-60 minutes to work)
- IV Amiodarone? - only if lidocaine not successful (need to pre-medicate with antihistamines/steroids)
Types of bradyarrhythmias?
Sinus bradycardia Sinus arrest Atrial standstill Sinoventricular rhythm (hyperkalaemia) AV block
What underlying factors must be identified and excluded for bradyarrhythmias?
High vagal tone e.g. GIT disease, CNS
Hyperkalaemia
Hypothyroidism
Drug side effects
When is atrial standstill seen? What happens? What is seen on ECG?
Hyperkalaemia e.g. Addison’s disease, urinary obstruction, oliguric/anuric renal failure
Sino-ventricular rhythm (SAN still drives the rhythm, atrial myocardium bypassed, so may be variable R-R like sinus arrhythmia)
Absent P waves, spikes T waves, mild prolonged QRS complex (atrial myocardium most susceptible)
Ventricular escapes
What are the types of AV block?
First degree AV block:
- P:QRS = 1:1
- Long P-R interval (>0.13s in dogs)
- Exclude high vagal tone and drug effects e.g. digoxin
2nd degree AV block:
- Mobitz I (Wenckebach phenomenon): vagal? increasing P-R interval then not conducted?
- Mobitz II: usually pathological, fixed P-R interval, randomly non conducted P wave
Third degree AV block:
- No relationship between P and QRS
- Dogs: medical treatment not likely to help
- Cats: may have faster escape rate (100-120bpm), may be asymptomatic)
Treatment of bradyarrhythmias?
Exclude/treat underlying disorders e.g. hyperkalaemia, hypothyroidism
Vaguely mediated? Atropine response test: expect >50% increase in HR after 30-40 mins
Oral medication:
- Anticholinergics e.g. Propantheline
- B2 agonists e.g. terbutaline
- Xanthine derivatives e.g. Theophyline
Life threatening: B2 agonist e.g. terbutaline
Methods of measuring BP?
Direct method: mostly anaesthetised patients, catheterise an artery Indirect methods (cuff 30-40% circumference of limb): - doppler technique: probe placed over underlying vessel, cuff inflated until can no longer hear flow, then reduce until can just hear it again and read SAP - oscillometric technique: more automated, gives MAP, SAP and DAP, take 5 readings, not v good if fidgety animal as affected by movement or if AF
Normal BP for dogs and cats? When classed as systemic hypertension?
Dogs: 130/75mmHg (sighthounds have higher BP 150/90)
Cats: 125/80 when relaxed
Systemic hypertension:
-systolic: > 160/175/180 (various definitions)
-diastolic: > 95-100
Diseases associated with secondary systemic hypertension?
Chronic renal disease Hyperthyroidism (cats) Hyperadrenocorticism Diabetes mellitus Liver diseases Hypothyroidism Acromegaly Phaeochromocytoma Hyperaldosteronism Chronic anaemia (cats) Obesity CNS disease
Consequences/manifestations of systemic hypertension?
Ocular - retinal haemorrhage, hyphaema, retinal detachment, blindness
CNS - seizures, dull and depressed, bad tempered, overt neurological deficits
Renal - failure, proteinuria
Cardiac - pressure overload causes concentric LV hypertrophy, heart murmurs may be due to LVOTO or MR
If systemic hypertension diagnosed, how to check for end-organ damage?
Examine retinas
History and neuro exam
Check urine SG and urine protein:creatinine ratio (UP:C) (normal <0.2)
Echocardiography/ECG
- concentric hypertrophy? (need to exclude SHT before diagnosing primary HCM in cats)
- arrhythmias due to myocardial hypoxia
- accelerated course of myxomatous degenerative valvular disease (dogs).
- high velocity MR jet (Doppler)
Search for underlying cause as primary hypertension rare in dogs and cats
Treatment of systemic hypertension?
If severe (SBP>200mmHg) treat before any other investigations (esp in cats to prevent retinal detachment or CNS bleeds)
Amlodipine (Ca channel antagonist with just vascular effects), check BP after 1 week, up-titrate if required
Identify and treat primary cause if possible
Protect kidneys:
- need to reduce GCP to reduce protein loss and further loss of nephrons
- ACE-I (benazepril): greater effect on efferent arteriole so reduce GCP, used with amlodipine to be significant
- telmisartan (ANG II receptor blocker)
What are the 3 factors of Virchow’s triad, leading to thromboembolism?
Circulatory stasis
Endothelial injury
Hyper-coagulable state
Feline Arterial Thrombo-embolism (FATE) - when happens? Appearance on echo?
Any condition resulting in stasis of flow in heart may result in thrombus formation
Usually in LA
‘Smoke’ on echo
Embolisation to any region - often distal aorta
Results in severe clinical signs (e.g. hindlimb paralysis), pain
Emergency presentation
Treatment of FATE?
Priority: analgesia and anxiolytic
- methadone, buprenorphine, morphine,
- aspirin; (ACP)
Consider “clot busting” drugs
- tissue plasminogen activator (tPA) - only if <6–12 hours of event
Stabilise underlying heart failure if present
Inhibit further platelet aggregation and activation
- clopidogrel, aspirin, heparin (cyproheptadine?- anti- 5HT)
Prevent collateral vasoconstriction caused by thromboxane, serotonin etc
- aspirin, cyprohepatidine
Prognosis is grave: need to warn owner that optimistic survival rate is 50%….
Prevention of FATE in at risk cats?
Aspirin at low dose
Clopidogrel (FATCAT study: Clopidogrel better than aspirin at reducing further events/improving survival)
Low molecular weight heparin (LMWH) e.g. dalteparin
Treat cardiac disease as appropriate
Difference between using Heparin vs LMW Heparin to prevent FATE?
Unfractionated Heparin:
- major effect on interaction of thrombin and antithrombin III
- Heparin-ATIII also inhibits factor Xa and other factors of coagulation cascade
- can over do it
- monitor APTT – increase x 1.5 - 2 fold
LMWH:
- Anti-Factor Xa
- do not need to monitor coagulation times
- can train owners to inject once or twice daily
Arterial Thromboembolism in dogs? When seen? Where common? Clinical signs?
Cavaliers pre-disposed?
Canine ATE only rarely associated with heart disease
More commonly associated with an endocrinopathy e.g. Cushing’s disease, Hypothyroidism.
Also commonly affects distal aorta, poss only one limb
Dogs present with hindlimb weakness or pain, worse with exercise
Pale/pulseless /cold compared with non-affected limb
What can cause pulmonary hypertension?
Pulmonary vascular changes (e.g. retained foetal vasculature) -> pulmonary hypertension -> right to left shunting across congenital heart defects (VSD / ASD / PDA) (Eisenmenger’s physiology)
Vascular changes associated with heart worm (Dirofilariaisis / Angiostrongylosis)
Pulmonary thromboembolism
Left sided heart failure (e.g. severe MR)
Primary severe respiratory conditions
Diagnosis of pulmonary hypertension?
Loud S2, loud TR murmur
Radiographs - dilated, tortuous or pruned pulmonary arteries
Doppler echo - dilated hypertrophied RV, dilated radiographic trunk, high velocity TR/PR jets
Treatment of pulmonary hypertension?
Treat underlying disease
Pimobendan?
Sildenafil (phosphodiesterase V inhibitor)
PTE prevention
Heartworm - species? Intermediate host? Clinical signs?
Dirofilaria immitis
Mosquitoes
Cor pulmonale, weight loss, fatigue, cough, dyspnoea
Life cycle of D immitis?
Microfilariae in dog’s blood
Mosquito ingests microfilariae during blood meal
Mature into L3 in mosquto
Introduced to dog when vector feeds
Migrate to right side of heart and mature into males and females
Female worms produce microfilariae after 6 months?
Dirofilariasis caval syndrome?
Needs worms removing
Don’t break worms as can cause anaphylactic shock
Diagnosis of D immitis?
Demonstrate circulating microfilariae - direct smear, microfilaria concentration tests
Heartworm Ag tests - detects mature females
Ab tests
Preventatives for Dirofilaria?
Selamectin monthly topical
Milbemycin (with praziquantel) monthly po
Moxidectin (with imidacloprid) monthly topical
Melarsomine Dihydrochloride - adulticide
What bacteria can be transmitted by Dirofilaria? Role in HWD? Treatment?
Wolbachia - obligate, intracellular, G-ve, endo-symbiotic bacteria
Found in uterus of female D immitis
May play role in pathogenesis of HWD - poss through their metabolites
Treat with Doxycycline prior to melarsamine
Angiostrongylus vasorum - size? hosts? Clinical signs?
Adults about 2cm long Dogs and foxes Intermediate hosts: slugs/snails Often young dogs may be asymptomatic - depends on worm burden and immune response Respiratory signs: chronic, unresponsive cough, pulmonary hypertension, dyspnoea Coagulopathy: haemoptysis, haematemesis Ill-thrift, exercise intolerance, CHF Subcutaneous & retinal haemorrhages neurological: paresis, ocular changes
Diagnosis of Angiostrongylosis?
Thoracic radiography
- cor pulmonale
- variable/patchy/mixed pulmonary infiltrates (often more marked at the periphery of the lung field).
Eosinophilia
Raised B-globulins
Angio Detect SNAP test (for antigen)
Larvae in faeces (Baermanns) or sputum (L1 0.4mm long, curved tail with dorsal spine)
Treatment of Angiostrongylosis?
Fenbendazole - slowly kills over 36hrs (not licensed against Angiostrongylus, but commonly used)
Milbemycin Oxime (with praziquantal)
Moxidectin (with imidacloprid).
Prednisolone if pulmonary changes severe (anaphylaxis)
Prognosis generally good unless pulmonary haemorrhage or worm burden very severe
Preventatives:
Moxidectin, Milbemycin (Milbemax) (q 4 weeks)
