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
