1
Q
Congestive heart failure clinical signs, what is the most important clinical sign
A
- Early ○ ↓ exercise tolerance ○ Tachypnoea with exertion - Then ○ Increased sleeping respiratory rate (should be less than 30 breaths per minute) - MOST IMPORTANT SIGN OF CHF § Used to decide whether treatment is working or not as well ○ Elevated resting RR - Finally ○ Dyspnoea ○ +/-Moist cough ○ Lethargy, anorexia Many dogs with significant pulmonary oedema do not cough
2
Q
Congestive heart failure what are some less common clinical signs
A
○ Acute onset severe LSCHF with no prior signs
§ Chorda tendinea rupture - significant murmur
○ Syncope (fainting - lack of oxygen to the brain)
§ Severe coughing
§ Cardiac tamponade - rare cause
□ LA tear
§ Myocardial failure
§ Pulmonary hypertension -> decreased oxygen to the brain
§ Tachyarrhythmias
§ Atrial fibrillation- irregular QRS interval, no p waves, sometimes f waves
○ Ascites -> RSCHF (tricuspid)
○ Cardiac cachexia - heart working harder, required more energy however not eating as feeling unwell - breakdown muscle
3
Q
Left sided congestive heart failure what are the general clinical presentations
A
○ CHF (wet): § Usually high-grade murmur (4-6/6), loud S1. § Tachycardia § Tachypnoea, dyspnoea § +/-crackles, wheezes - need large amount of fluid § Brisk pulses § Pale MM (hypoxia) - CO output poor, so vasoconstriction to preserve blood flow to essential areas § Cyanosis (severe hypoxia) ○ Low output signs (cold): § Low temperature § Cool extremities § Weak pulses § Slow CRT
4
Q
Right sided congestive heart failure physical examination presentation
A
○ +/-tricuspid murmur ○ Ascites ○ +/-Jugular distention ○ Jugular pulses ○ Hepatojugularreflux ○ SQ oedema (rare) ○ Pleural effusion (rare)
5
Q
What are 9 diagnostic techniques for Myxomatous (mitral) valve disease (MMVD)
A
- Signalment
- History
- Clinical signs
- PE
- Thoracic radiography
○ Assess LA size
○ Evaluate lungs for LSCHF
§ oedema, +/-venous congestion
○ RSCHF- CVC distention, hepatomegaly, pleural fissure lines - Blood pressure
- echocardiography - confirm diagnosis, assess contractility, severely - LA size, large dog echo
- lab testing - electrolytes and renal parameters, hydration
- +/- ECG only if arrhythmic
6
Q
What are the 4 stages of Myxomatous (mitral) valve disease (MMVD), what defines these
A
Stage A
- At risk for developing disease
- Cavillers king Charles spaniel - NEED TO MONITOR FOR MURMUR
Stage B
- Structural heart disease (murmur) present but no clinical signs
- B1: no radiographic or echocardiographic evidence of cardiac remodelling
- B2: Hemodynamically significant, with evidence of remodelling (heart enlargement) on imaging
Stage C - in congestive heart failure
- Past or current signs of congestive heart failure
- May include some dogs requiring advanced stage D treatments from first onset of failure
Stage D
- Clinical signs of heart failure are refractory to ‘standard therapy’
7
Q
Myxomatous (mitral) valve disease (MMVD) treatment in preclinical stage A
A
○ Client education ○ Disease prevalence ○ Clinical signs § Exercise intolerance § Cough § Tachypnoea ○ Annual checks NO survival benefit with any drugs
8
Q
Myxomatous (mitral) valve disease (MMVD) treatment in stage B1 and B2
A
- Stage BI (valve disease, heart normal size)
1. Client education
§ Risk of failure
□ 30%most small breeds
□ Often takes years
§ Clinical signs
2. Baseline radiographs (or echo)
3. Weight loss if overweight
4. Mild salt restriction
5. Periodic monitoring
§ Sleeping RR at home(< 30/min)
§ Check-up q 6-12 months - Stage B2 (cardiomegaly)
1. Pimobendan - delays LSCHF or cardiac death (by 15 mo)
- reduces risk of LSCHF or cardiac death (by 1/3)
9
Q
Myxomatous (mitral) valve disease (MMVD) treatment in stage C
A
- Stage C, Mild-moderate CHF
1. Drain ascites/pleural effusion directly
2. Decrease preload (atrial filling pressure)
§ Reduce blood volume
□ Diuretic (furosemide)
□ ACE Inhibitors
□ Moderate salt restriction, avoid salt loading
3. Control neurohormonalactivation
§ ACEI, +/-spironolactone, pimobendan
4. Reduce mitral regurgitation
Pimobendan - vasodilator as well - PROLONGS SURVIVAL
10
Q
Myxomatous (mitral) valve disease (MMVD) treatment for stage D
A
Stage D - severe/refractory CHF Oxygen, sedate, cool, minimal stress. - As for milder disease plus: ○ Diuretics § Higher dose/frequency IV § combination therapy (add spironolactone) ○ Reduce preload § venodilator ○ Tachyarrhythmias § Control HR ○ Reduce afterload § Arterial vasodilator § Keep BP > 100mmHg ○ If low output signs § Additional positive inotropes § Care with vasodilator/diuretics § Consider PHT ○ Greater sodium restriction
11
Q
What are some complications of treatment for Myxomatous (mitral) valve disease (MMVD) and monitoring
A
Complications of therapy - Prerenal azotaemia - Hypotension and renal injury - Hypokalaemia - Compliance ○ Too many pills! ○ PU/PD, incontinent - (never restrict water) Monitoring - 1-2 weeks after discharge - q 3-6 months if stable - More frequent for severe cases
12
Q
Prognosis for congestive heart failure in most small breeds, CKCS and large breeds
A
- Most small breeds ○ Progression over years ○ Only 30% CHF ○ Median survival after CHF 6-10 mo - CKCS ○ Usually CHF within 1-2 yrsof murmur detection ○ 30% mortality within 3-4 y - Large breeds also usually progress more quickly
13
Q
Primary cardiomyopathies what is it and list 5 main ones, what all called and how to diagnose
A
- Primary abnormality of the cardiac muscle: ○ Dilated cardiomyopathy (DCM) ○ Hypertrophic cardiomyopathy (HCM) ○ Arrhythmogenic right ventricular CM ○ Restrictive CM ○ Unclassified CM - ALL CAUSE POOR RELAXATION OF THE VENTRICLE - Diagnosis of exclusion
14
Q
Secondary cardiomypathies what are they, causes and what need to treat
A
- Secondary dilated cardiomyopathy: ○ Doxorubicin (toxins) ○ Trauma ○ Tachycardia-induced ○ Taurine deficiency ○ Hypothyroidism (dogs) ○ Myocarditis ○ Infarction (embolisation) - Treat the primary disease!
15
Q
Canine dilated cardiomyopathy (DCM) what is the primary problem, causes and pathogenesis (how leads to failure)
A
- Primary progressive decline in contractility
○ Myocardial failure = systolic dysfunction - Multiple genetic factors
Pathogenesis
-> decrease contracility, decrease output -> SNS, RAAS -> AV regurg, eccentric hypertrophy ->
Decrease contractility -> compensated via dilation - Dilation -> pulls apart of the mitral valve
Systolic cardiac failure -> CHF, output failure (more likely to present with exercise intolerance and lethargy
16
Q
Canine dilated cardiomyopathy (DCM) signalment, presenting sign and cardiac finding
A
- Signalment ○ Large-giant pure breeds - Doberman pinschers § Highest prevalence of DCM § Usually present 5-7 years old § Autosomal dominant □ Males present earlier/more severely § Long preclinical phase (2-4 yrs) -> may not hear murmur for awhile ○ Some spaniels ○ Middle aged-older ○ Males - Presenting signs ○ Sudden death ○ Syncope ○ CHF (L > R) - Cardiac findings ○ Tachyarrhythmias common - due to large breed dogs ○ Mitral murmur
17
Q
Doberman pinschers DCM prognosis, why and how to pre-screen
A
- Guarded to grave prognosis ○ 20%-40% sudden death ○ Ventricular arrhythmias and syncope § More sudden death ○ Severe LSCHF § Most dead within 3 mo □ Sudden death or □ Refractory heart failure ○ Bilateral failure -> MST 3 weeks Preclinical screening 1. Echocardiography - best § Reduced contractility □ Overt DCM 2-3 yrs 2. 24-hour ECG (Holter) - if don’t detect on ECG § 50 VPCs in 24 hrs+/-couplets, triplets § Diagnostic for DCM
18
Q
Boxer cardiomyopathy what is the most common one, what occurs, cause and clinical signs
A
Arrhythmogenic right ventricular cardiomyopathy - MOST COMMON
- Change in right ventricle -> fibro-fatty infiltration
Cause - Genetics
○ Familial
○ Autosomal dominant
○ Screen from 3 yo
- Clinical signs
○ ventricular arrhythmias - can be quite severe
○ Syncope episodes - if having these in this breed ECG
○ exercise intolerance
○ right heart failure
- sudden death - higher risk
19
Q
Arrhythmogenic right ventricular cardiomyopathy what breed most common in, what are the 3 categories, clinical signs and prognosis
A
Boxer Category I: Concealed - Mild ventricular arrhythmias without clinical signs - Do well 2 years or more Category 2: Overt - Syncope, moderate ventricular arrhythmias. - Can do well for years with antiarrhythmics (beta blockers - sotalol) Category 3: Myocardial failure - As for 2, plus: - echo changes of poor systolic function - 50% present in CHF Likely to die of CHF or die suddenl
20
Q
American cocker spaniels what mostly present as, what is the common cause and therefore treatment, follow up and prognosis
A
- Usually present in CHF
○ Treat heart failure
○ Treat with oral taurine and carnitine - hoping this is the cause - Follow up
○ Improved function by 3-6 mo on echocardiography
○ Once demonstrated -> Wean off cardiac drugs - Usually clinical recovery!
21
Q
Irish wolfhounds what generally present as with heart and cause
A
- Autosomal recessive inheritance
- 2 presentation
1. Classic DCM
§ Biventricular failure
2. Atrial fibrillation with slow ventricular response
§ Asymptomatic at the start
§ May progress to CHF (3-4 years
§ DDx‘benign’ AF
□ (healthy!) heart on echo
22
Q
DCM diagnosis what are the 3 techniques
A
1) Radiography ○ LSCHF(pulmonary oedema) - large left atrium ○ RSCHF(ascites, pleural effusion) ○ Usually generalised cardiomegaly 2) Echocardiography - Essential to confirm diagnosis ○ Usually LV + LA dilation ○ +/-RV/RA dilation ○ Systolic dysfunction § Fractional shortening < 15-20% 3) labwork - Biochemistry ○ Pre-renal azotaemia § low cardiac output ○ Hyponatraemia § Dilutional in severe CHF - NT-proBNP
23
Q
What are some clinical signs for severe pulmonary oedema or low output (forward) failure due to primary cardiomyopathies
A
- Hypothermia
- Weak peripheral pulses
- Pale MM, slow CRT
- Cold extremities
+/- - Quiet heart sounds
- Mitral/tricuspid murmur
- Tachyarrhythmias
- Congestive signs
24
Q
DCM treatment what are the 3 main aims and 2 treatments for preclinical DCM in dobermanns ALSO what need to control in all stages
A
AIMS 1. Control signs of CHF 2. Increase survival time 3. ↘ risk of sudden death Preclinical (occult) DCM Dobermanns - no CHF yet 1. ACEI - ace inhibitors ○ slow progression of ventricular remodelling ○ Delay CHF 2. Pimobendan ○ Delay onset clinical signs ○ Prolong survival Control arrhythmias/HR at all stages of disease
25
DCM treatment for mild/moderate and severe CHF
Mild-moderate CHF (furosemide, ACEI +) - know in this due to tachypnoea (same as previous lecture)
1. Pimobendan
○ Improved survival time over ACEI and furosemide alone
○ +/-spironolactoneto limit fibrosis and remodelling
- Pimobendan adds up to 9 months!
Severe CHF
1. Lots of furosemide
2. Nitroprusside
○ Don’t over-vasodilate as poor CO (don't want too low BP)
3. Lots of inotropicsupport
○ Start pimobendan (IV/PO)
○ +/-Dobutamine CRI
4. ACEI when stable - long-term treatment
26
DCM prognosis after onset of CHF and cocker spaniels
- Poor after onset CHF
○ Sudden death can occur any time
○ Historically few weeks (Dobies) or months (others)
○ Good early response = longer survival
- Better with Pimobendan!
- Best for cocker spaniels if taurine deficient - can go back to normal
27
What are the 3 main causes of dyspnoea in cats and therefore what need to be careful of
1. FBD - feline asthma
2. CHF - congestive heart failure - DON'T GIVE FLUIDS - important for stabilisation need to rule this out
3. Pyothorax
28
Feline cardiomyopathies what is the most common types and how differ from dogs
```
- Primary cardiomyopathies
○ 62% of feline heart disease:
§ Hypertrophic (2/3)
§ Restrictive
□ First two - DIASTOLIC FAILURE
§ Unclassified
§ Dilated - rare due to taurine in all cat foods
§ ARVC (< 1%)
- Differences from dogs:
○ “Acute” presentations common - without clinical signs
§ CHF
§ Aortic thromboembolism
§ Sudden death
○ LSCHF -> Pleural effusion common
§ Usually modified transudate
§ Chylothorax
```
29
In terms of cat what supports cardiac origin in terms of clinical signs
- Normal to Low rectal temperature
- Murmur? - can get physiological cause in the exam room - stress
- Gallop rhythm
- Arrhythmia
- Bradycardia (or tachycardia)
- CAN HAVE NO MURMUR OR CLINICAL SIGNS AND BE IN HEART FAILURE
○ Echo important to diagnose in cats however need to be careful if in heart failure
- NTproBNP - snap blood test
< 100 pmol/L: normal
< 270 pmol/L: unlikely
>270 pmol/L: likely
30
Feline dilated cardiomyopathy what are the 2 main causes and prognosis and treatment
```
Causes
1. Taurine deficiency - rare
○ Exceedingly rare now
○ Measure levels
○ Supplement
§ Improve clinically 3 wks
§ Echo improves 2-4 mo
- Idiopathic? - more commonly
○ Poor prognosis
○ Pimobendan - OFF-LABEL
```
31
Feline hypertrophic cardiomyopathy (HCM) what results in, causes and what need to exclude
```
- PRIMARY LV concentric hypertrophy
○ Genetics + environment
○ Autosomal dominant
§ Maine coon, Ragdoll
§ Prognosis worse if homozygous
○ Males affected earlier/more severely
Need to Exclude SECONDARY hypertrophy:
○ Hyperthyroidism
○ Hypertension
○ (Acromegaly)
```
32
Feline hypertrophic cardiomyopathy pathogenesis and clinical presentation with common and uncommon signs
Pathogenesis
-> protein defect -> ventriicle concentric hypertrophy -> stiff ventricle, diastolic relaxation imparied -> SNS, RAAS, LVOT obstruction -> progression to CHF
Clinical presentation
- murmur (2/3)
- gallop rhythm (1/3)
- arrhytmia
- CHF - usually acute
- other signs same as dog - tachypnoea, dyspnoea, lethargy, cough (sometimes
- ALSO - aortic thromboembolism (common) - cold extremities and PALE, not painful
- high risk of recurrence
- uncommon signs - weakness, sudden death
33
Feline hypertrophic cardiomyopathy what are the 3 main diagnostic techniques and the findings
```
Radiography
- Mild
○ Normal
- Advanced
○ Classic is ♥shape
§ Large LA and auricular bulge
○ Pleural effusion and/or pulmonary oedema
2. ECG
○ Arrhythmias
○ Left axis deviation
○ Not specific
3. Ultrasound -> essential for diagnosis
- Increased diastolic wall thickness ≥ 6mm
- +/-large LA
- Diastolic dysfunction
- SAM +/-LVOT obstruction
```
34
Feline hypertrophic cardiomyopathy treatment for pre-clinical and clinical acute
```
- Pre-clinical
○ No evidence any drugs prolong survival
○ Some use β-blockers for severe LVOT (left ventricular obstruction
○ Check annually
- Clinical –acute
○ O2, furosemide
○ Thoracocentesis!
○ Pimobendan onlyfor refractory CHF
○ Thromboprophylaxis if large LA +/-thrombosis
§ Clopidogrel
```
35
Feline hypertrophic cardiomyopathy treatment when stable and when not to give beta-blockers
```
- When stable
○ ACEI
○ Beta-blockers for severe LVOT obstruction
○ Avoid corticosteroids - can worsen and bring on heart failure due to altered fluid dynamics
○ Limit stress
- DO not give beta-blockers if
○ Hypotensive
○ Bradycardic
○ In CHF
○ Thromboembolism
```
36
Feline hypertrophic cardiomyopathy monitoring and prognosis
```
Monitoring
- Resting RR at home (<30)
- Recheck at 1-2 weeks then q 3 monthly
○ Renal parameters (if in renal disease need to be careful for diuretics as need MORE volume for renal disease and less for heart disease)
○ Electrolytes
○ BP
- ECG/echo q 6-12 months
Prognosis
- Variable
- Worse if more severe echo changes
- Median survival
○ Asymptomatic 1129 days
○ CHF 563 days
ATE (aortic thromboembolism disease) 248 with clopidogrel
```
37
Pyothorax in cat what important clinical sign, how to diagnose, once diagnosed treatment and treatment once stable
fever - need to confirm diagnostically via thoracentesis also help relieve (fluid send for culture and sensitivity -> need to request anaerobic culture (important for bacteria in mouth oral cavity))
○ Pyothorax STINKS chylothorax - doesn't smell -> need to analyse and look under microscope (degenerate) to confirm
§ Once diagnosed ->antibiotics (amoxicillin - broad-spectrum) - continue for 6 weeks and change based on culture if needed
§ Once stable -> anaesthetise or sedate to place on thoracic drain
38
Arterial blood gas what are the 2 questions that are important to ask and how to determine the answer
1. Hypoxic or not?
- Are they below Pao2 80-100
2. Is it due to hypoventilation or lung issue or both
IF PaO2 and PaCO2 is low (still able to diffuse) then gas exchange issue
If PaO2 decreased and CO2 increased then hypoventilation
○ If Pa2 is low to the same amount that CO2 is higher than hypoventilation is the issue
39
Rat bait arterial blood gas findings and why
- Hypoventilation -> DOESN'T MEAN NOT HIGH RESPIRATORY RATE
○ Can be rapid RR BUT shallow - low ventilation volume -> in this case as haemothorax so unable to fill lungs
○ ALSO - gas exchange issues as bleeding into the alveoli leading to gas exchange impairment
○ THEREFORE - gas blood probably PaO2 decreased about 60mmHg while PaCO2 is increased but not as much as PaCO2 has decreased (50mmHg) -> hypoventilation + gas exchange problem
40
What are the 6 common conditions that affect the upper airway
1. Brachycephalic obstructive airway syndrome (BOAS)
2. Laryngeal paralysis
3. Neoplasia
○ SCC of nasal planum, nasal ACA, laryngeal, tonsillar and tracheal neoplasia, polyps
4. Tracheal collapse
5. Fungal disease (nasal cavity)
6. Nasal FBs
41
Brachycephalic obstructive airway syndrome signalment and clinical signs
Signalment
- Pugs, Boston Terriers, English Bulldog, Pekingese, Shih Tzu, Boxer, French Bulldog
Clinical signs
- Inspiratory dyspnoea – exacerbated by exercise and increased environmental temperature
- ‘Snoring’ noise (stertor)
- Cyanosis, hyperthermia, collapse
42
Brachycephalic obstructive airway syndrome pathophysioogy - why is there an issue
- Compression of nasal passages and distortion of pharyngeal and laryngeal tissues due to brachycephalic anatomy →
- Increased resistance to air flow in upper airway
○ Stenotic nares (50-85% cases)
○ Elongated soft palate (80-100% cases)
○ Eversion of laryngeal saccules (2o change) -> due to large negative pressure - oedema - blocking the airway
○ Laryngeal collapse (advanced 2o change)
○ Tonsil eversion - not really related so shouldn't be removed in surgical treatment
43
Brachycephalic obstructive airway syndrome what are the 2 main concurrent conditions and signs of these
1) Hypoplastic trachea (English Bulldogs)
○ Tracheal diameter : Thoracic inlet diameter (TD:TI)
§ English Bulldogs TD/TI = 0.116
§ Other brachycephalic breeds TD/TI = 0.157
§ Non-brachycephalic breeds TD/TI = 0.208 - 20% trachea diameter:thoracic inlet
2) Gastrointestinal disorders
○ Dysphagia, vomiting (75% BOAS cases)
○ Severity of GI signs related to severity of URT signs
○ Rx: antacids (omeprazole) and prokinetics (cisapride)
44
Brachycephalic obstructive airway syndrome diagnosis and initial management
Diagnosis
1. Typical anatomy and breed
- Usually diagnosed in patients 2-3 years old
2. Clinical signs
○ Inspiratory dyspnoea, exercise intolerance, vomiting / regurgitation, hyperthermia
3. Examination of upper airway under light plane of anaesthesia - want to measure soft palate length and laryngeal saccules or collapse
Initial management
- Decrease airway turbulence and airway inflammation
- Minimize stress
- Cool environment
- Supplemental O2
- IV short acting corticosteroid
- Sedation (acepromazine / butophanol)
45
Brachycephalic obstructive airway syndrome surgical correction what are the 3 surgical techniques that needs to occur
1) resection of stenotic nares - vertical or horizontal wedge resection with scalpel blade
2) soft palate resection (staphylectomy) - soft palate needs to just touch the epiglottis
3) removal of everted laryngeal saccules - Grasp with tissue forceps and cut at the base with mezzembarb scissors - note that severe haemorrhage
46
Soft palate resection (staphylectomy) what are the surgical landmarks, and how to perform, what equipment makes it better
○ Surgical landmarks:
§ Caudal pole of tonsils - landmark for the epiglottis
§ Tip of epiglottis
○ Place stay sutures at margins and in tip of elongated soft palate
○ Sharp incision and suture oral mucosa to nasal mucosa - need to suture to prevent scar tissue formation and haemorrhage
○ Laser - ↓ haemorrhage, swelling, surgical time -> don't have to suture if use laser
47
What is a secondary sign of Brachycephalic obstructive airway syndrome the 3 stages, and treatment at this stage
Laryngeal collapse - secondary sign of BOAS
- Laryngeal collapse - Loss of cartilage rigidity
Stage I - Everted laryngeal saccules
Stage II – Aryepiglottic folds deviated medially and obstruct ventral aspect of glottis
Stage III – Corniculate process of arytenoid cartilages deviate medially
Hard to surgically treat at this state -> stent on-top of arytenoid to prevent collapse
48
Brachycephalic obstructive airway syndrome once undergone surgical management what post op care is needed
Post op care
- Perioperative IV corticosteroids - NOT NSAIDS
- Acepromazine – anti-anxiolysis - if they are excitable
- Delay extubation as long as possible
- Oxygen supplementation
- Analgesics
- Temporary tracheostomy may be required if lots of oedema around soft palate (unable to breath from airway)
- Withhold food for 18-24 hours post surgery
49
Brachycephalic obstructive airway syndrome prognosis and complications
- Good to excellent outcomes in ~ 95% cases - except stage 3 laryngeal collapse
- Complications uncommon
○ Post op swelling, haemorrhage
○ Excessive soft palate resection → nasal regurgitation
○ Aspiration pneumonia
○ Dehiscence of nares repair
○ Voice change (excessive scaring following sacculectomy)
○ Persistent upper airway noise - will never be NORMAL
50
Laryngeal paralysis what are the 3 main causes
```
1. Congenital
○ Bouvier des Flandres, Siberian Huskies, Dalmations
○ Dx < 1 year old
2. Acquired
○ Labrador, Golden Retriever, Saint Bernard, Irish Setter
○ Older dogs (>9 years)
○ Damage to recurrent laryngeal nerve
§ Dog fights
§ Surgery (thyroidectomy)
§ Mediastinal or cervical masses
○ Polyneuropathy
3. Idiopathic most common
```
51
What are 6 differentials for stridor
- Laryngeal paralysis
- Neoplasia on the larynx - obstruct the area
- Laryngitis, oedema
- Laceration of cartilage
- Laryngeal collapse
- Thyroid carcinoma
52
Laryngeal paralysis clinical signs
- Voice change, Stridor, exercise intolerance
- Coughing / gagging after eating / drinking
- Slowly progressive over months to years
- Male dogs 2-3 X more common than females
- Hyperthermia / Heat stroke – Spring / Summer
- Dysphagia / megaoesophagus
- Aspiration pneumonia
53
Laryngeal paralysis diagnosis 2 main things and what doing them for
1) Thoracic radiographs to rule out:
- Mass obstructing airway, Aspiration pneumonia - if also present need to treat first
○ Megaoesophagus - risk factor for surgery
§ Complication rate ↑↑ with megaoesophagus
2) Laryngeal exam under light plane of anaesthesia:
○ low dose propofol, Thiopental - no sedation before
- Need to observe movement -> Normal movement is to abduct arytenoid cartilages and vocal folds during inspiration
§ (i.e. when you breath in, airway needs to be opened)
□ Abduct – move AWAY from the midline
□ Adduct – move TOWARDS the midline
○ No movement during inspiration or paradoxical (mechanical) movement → Laryngeal paralysis
○ If no movement but maybe anaesthesia issue -> Doxapram will increase respiratory effort and intrinsic laryngeal motion so will then examine again
54
Laryngeal paralysis treatment, goal and steps to perform
- Goal of surgery to open the rima glottis area to decrease airway resistance:
- Unilateral arytenoid lateralization (Preferred)
1. Skin Incision made ventral to the jugular vein
2. Section through skin and subcutaneous muscle
3. Feel the ring of the thyroid cartilage - abduct and excise thyropharyngeal muscle (allows placement of suture)
4. Reach articulation between cricoid and arytenoid cartilage -> need to excise the cricoarytenoids muscle to gain access
5. First bite through dorsal and caudal of cricoid - small haemostat to elevate, other bite in muscular process of the arytenoid - NOT TOO TIGHT - could cause opening to be too large which predisposes to aspiration pneumonia
55
Laryngeal paralysis post operative considerations and complications
- Important to have appropriate aftercare available for these patients.
- 24 hour ICU monitoring with oxygen source
- Ice cubes and meatballs post op
- Use chest harness instead of collar (don't want to touch neck)
- Post op complications:
○ Seroma formation (most common)
○ Suture breakage
○ Life-long risk of aspiration pneumonia
56
Tracheostomies what required for, what does it provide, what does it need, placed where and the 3 steps in the technique
- May be required as adjunct to BOAS or any upper respiratory tract obstruction that is life threatening (ie, snake bite)
- Provides temporary airway
- Needs constant 24hr care
- Place between 2-5th rings
Technique
1. Open skin and subcutaneous around 2nd and 3rd tracheal ring
2. Incise the tracheal ring and place stay sutures cranial and caudal to tracheostomy site
○ Stay sutures enable easy access to incision site and able to flush and place new tube in if need be
3. Then place the tracheostomy within
57
Permanent tracheostomy what are the 3 indications, risks and how to perform
- Indications:
○ Laryngeal collapse
○ Laryngeal paralysis
○ Laryngeal neoplasia
Risks of drowning, aspiration pneumonia, Hyperthermia
1. Suture sternohyoideus muscles dorsal to trachea to bring trachea closer to skin
2. Ventral window 3-5 rings length, central 1/3
3. H shaped mucosal incision
4. Suture mucosa to skin
58
Neoplasia of the upper airway what are the 3 main forms, treatment options within
```
1. Nasal planum tumours
○ SCC → Nosectomy in cats, cryotherapy
2. Adenocarcinoma (ACA) of nasal cavity
○ Dx with core biopsy, CT imaging
○ Radiation therapy +/- surgery
3. Laryngeal and tracheal neoplasia
○ Rare
○ Voice change, cough, exercise intolerance
○ Biopsy
○ Tracheal resection - permanent tracheostomy may be needed
```
59
List 7 main conditions of the thorax that require surgery or thoracic drainage
```
1. Thoracic wall conditions
○ Trauma (HBC, dog fights → rib #, flail chest)
○ Rib/ thoracic wall neoplasia
2. Diaphragmatic hernia
○ Traumatic (acute vs chronic)
○ Congenital (PPDH)
3. Pleural disease
○ Chylothorax
○ Pyothorax
4. Pulmonary pathology
○ Neoplasia, lung lobe torsion, bullae/blebs, lung abscess
5. Mediastinal disease
○ Mass-Thymoma,
○ Pericardial effusion
6. Correction of congenital cardiac or vascular ring anomalies (PRAA / PDA)
7. Oesophageal FB/ neoplasia
```
60
Thoracocentesis what indicated for and technique
- Thoracocentesis is indicated for relief of respiratory compromise and can provide samples for diagnostic testing.
- Thoracic drain placement may be required for recurrent pleural effusions or for pyothorax treatment.
Technique
- Positioned in sternal recumbency, get IV access, oxygenated and sedation (butorphanol - less respiratory depression)
- Prepare the area - clip and scrub and use sterile gloves
- 7th - 9th ICS
- Cranial to the rib in order to avoid intercoastal nerves
61
Thoracostomy tube placement what does it provide, what is required where place and how to place
- Continuous/ intermittent drainage of fluid or air from thoracic cavity
- Requires general anaesthesia after thoracocentestis
- Subcutaneous tunnel
- Enter 7th-9th intercostal space dorsal 1/3– 1/2
- Curved haemostats or trocar tube to place
- Direct tube cranially and ventrally
- 3 way tap, suture in place
- Take post tube placement thoracic radiograph
62
What are 8 indications for thoracotomy
1. Trauma (HBC, dog fights → rib #, thoracic wall)
2. Lung pathology (neoplasia, lung lobe torsion, bullae/blebs
3. Neoplasia (Ribs, Mediastinal masses
4. Correction of congenital cardiac or vascular ring anomalies (PRAA / PDA)
5. Thoracic duct ligation (Chylothorax)
6. Oesophageal foreign bodies
7. Pericardial effusion
8. Diaphragmatic hernia/PPDH
63
Thoracotomy what are the 4 approach, most common
1. Intercostal thoracotomy - common
○ Left intercostal thoracotomy
○ Right intercostal thoracotomy
§ Left 4th or 5th intercostal most common
2. rib section thoracotomy
3) median sternotomy - common - allows exposure or both sides of thoracic cavity - saw to cut through manubrium
4) trans-diaphgragmatic approach - midline abdominal approach, appraoch used for diaphragmatic hernia repair
64
Thoracosopy what does it do, what used for, is it safer than thoracotomy and what leads to
- Minimally invasive procedure to visualize pleural cavity and intrathoracic organs - small tube placed into small incision in chest
- Subtotal pericardiectomy, PRAA/PDA correction, Video assisted thoracic surgery (VATS) lung lobectomy
- Magnification and lighting
- Less morbidity than thoracotomy
- Pneumothorax → artificial ventilation required
65
Diaphragmatic hernia surgery when delay why and what are indications for urgent surgery
- Delay surgery if stable
○ Pulmonary contusions improve in 24-48 hours
○ Volume replacement for hypovolemic shock
○ Oxygen supplementation
- Indications for urgent surgery
○ Gastric herniation - as can continue to expand and take up area from lungs
§ Can possibly do GA and gastric tube to deflate the stomach
○ Continued haemorrhage and hypovolemia
○ Abdominal pain
66
Diaphragmatic hernia surgery what are the 5 steps in the process
1. Ensure wide clipping of thorax
2. Midline laparotomy
○ Can extend to caudal sternotomy if required
- Two main types of tear
○ Radial
§ Parallel to muscle fibres
○ Circumferential
§ Perpendicular to muscle fibres at rib attachment
○ Could also be a combination of the two
3. Replace abdominal organs from thorax into abdomen
4. Appositional continuous suture pattern with absorbable monofilament suture
○ Only freshen edges if D-hernia is chronic
5. Place thoracic tube to drain air
- Can have issues with closure of abdomen if chronic hernia
67
Peritoneopericardial diaphragmatic hernia what caused by, clinical signs, repair
- Congenital communication between abdomen and pericardial sac
- Commonly asymptomatic
- Repair as for traumatic
- Central defect - not in pleural space
68
Lung lobectomy what are 5 indications
- Lung laceration
- Lung lobe torsion
- Pulmonary neoplasia
- Lung abscess
- Lung Bulla/ blebs
69
Partial lung lobectomy when indicated and how to perform
if pathology at distal third of the lobe
1. Crushing forceps
2. 1 or 2 rows of continuous overlapping suture
3. Cut between sutures and the forceps
4. Suture over edge with continuous absorbable sutures
70
Total lung lobectomy when indicated how to perform
if pathology is higher than just distal third of lobe or neoplasia
Intercoastal - dorsal -> encounter artery, bronchi and then vein
- Ligature 3 for artery and vein -> transfixing suture should be used
Bronchi - isolate and double clumps, collapse with horizontal suture mattress suture
HAVE TO CHECK FOR LEAKS
- Flooding thorax with saline and check
71
Flial chest what is it, caused by, and treatment
- segmental fracture of adjacent ribs
- Fractured segment moves paradoxically with respiration due to intrapleural pressure changes
- Caused by trauma
○ Bite wounds, HBC, kick
- Generally non-surgical treatment
- Splint applied to chest wall with circumcostal sutures
72
Rib tumours diagnosis what are the 2 main types and MST
- Radiography
- CT scan to determine extent of disease and staging (lungs and LNs)
- Pre-operative biopsy (OSA vs. CSA)
1. Osteosarcoma
○ Most common rib tumour
○ MST 35-120 days Sx only
○ MST 240-290 days Sx + Chemo
○ ALP prognostic (↑ ALP → ↓ Px)
2. Chondrosarcoma
○ MST 1080-1750 days Sx only
- Chemotherapy not indicated
73
Rib tumour surgery what approach and how to remove
Intercostal approach
- Incision 1 ICS caudal to mass
- Palpate mass internally to determine margins
- 3cm dorsal and ventral to affected ribs
- 6 ribs maximum to be resected
- Latisimus dorsi muscle rotation flap
74
Frusemide what is it, function, how effective, minor effects and dose for pulmonary odedema
Loop diuretics
- Inhibits resorption of electrolytes in thick ascending loop of Henle and decreases resorption of sodium/chloride in distal renal tubule
- Most potent type of diuretic
- Most effective at treating oedema
- Other minor effects - IV vasodilatory affect can also have a cough suppressant activity
Dose - depends on severity of oedema
- Higher dose for large pulmonary oedema
- Most important thing -> monitoring the patient - are the clinical signs improving (resting respiratory rate)
○ Base the dose on response
1mg/lk iv - 12mg/kg
75
Frusemide onset of action, peak effect and duration of effect for IV and oral administration
- IV administration
○ Onset of action 5 minutes – Peak effects 30 minutes - response around 15-30mins
○ Duration of effect 2-3 hours
- Oral administration
○ Onset of action 60 minutes – Peak effects 1-2 hours
○ Duration of effect 6 hours
76
Pimobendan what are its affects and why used with congestive heart failure
- Positive inotrope: Calcium sensitiser and increases rate and extent of myocardial force
- Vasodilator: Phosphodiesterase III inhibition increases myocardial contractility and dilates systemic arterioles
- May also have effects on myocardial relaxation
- May have anti-inflammatory actions
- IMPROVES SURVIVIAL TIME
77
ACE inhibitors what congestive heart failure cases used in and benefits and give main example used
- Use in chronic cases
- Little benefit in acute setting as weak vasodilator effects and delay in onset
- NO TANGIBLE BENEFIT before development of CHF
Benazepril
78
Spironolactone what is it and function - what used for
- weak diuretic
- Blocks the aldosterone receptors in the cortical collecting duct (help those who become refractory to ACE inhibitors)
○ Blocking remodeling effects of aldosterone
- Aldosterone and angiotensin II "escape" from ACE-inhibitor suppression weeks to months after institution of therapy
- for use in congestive heart failure cases
79
Thiazide diuretics function, when use, what is possible issue
- Reduce membrane permeability in DCT to sodium and chloride
- For use in conjunction with frusemide if ineffective diuresis - last resort
- Mild-to-moderate diuretic
- Hydrochlorothiazide/ Chlorothiazide -> may push into renal failure
80
Dog - Congestive heart failure what is involved with continuing therapy
- Discharged after 24hrs
- Frusemide 3mg/kg PO q12hrs
○ Owner to monitor respiratory rate
○ Adjustments to therapy based on resp rate while sleeping (back below 30 breaths per minute)
- Pimobendan 0.3mg/kg PO q12hrs
- Benazepril (ACE inhibitor) 0.5mg/kg PO q24hrs
- Revisit in 7 days to monitor urea, creatinine & K+, month later then every 3 months if responding
81
DCM main goal of treatment and what old treatment, why bad and new treatment, what are the 3 things stabilised on
goal - relieve congestion
- Frusemide 2mg/kg i.v.
- Dobutamine - used to be used NOW USE PIMOBENDAN IV as VPC are common with dobutamine
○ Initially 2.5mcg/kg/min increased at 2.5mcg/kg/min increments to 10mcg/kg/min
○ blood pressure increased to a measurable 120mmHg systolic
○ Dog began to have multiple VPCs so reduced dose incrementally back down
○ VPCs continued and paroxysmal V-Tach developed
- Changed to oral pimobendan
- Stabilised on (with only intermittent VPCs):
1. 2mg/kg frusemide PO q12hrs
2.Pimobendan
3. ACEi
82
Arrhythmogenic Right Ventricular Cardiomyopathy (Boxer Cardiomyopathy) what is the goal with treatment and main risk, therefore treatment option and function
- Risk of sudden death
- Sympathetic tone worsens arrhythmia - TRY TO REDUCE SYMPATHETIC TONE
Treatment
Sotalol
-> Beta blocker
- non-selectively binds to both β1- and β2- adrenergic receptors preventing activation of the receptors
- Type III antiarrhythmic action
○ acts on potassium channels and causes a delay in relaxation of the ventricles - reduce chance of sudden death
83
What is important to consider with treatment of cats with heart failure
IN ALL CATS - reducing stress is important in the treatment
- If have pleural effusion - due to congestive heart failure
- > Need to remove pleural effusion will not be reabsorbed via diuretic medication
84
Cat - congestive heart failure long-term treatment and what is different with dogs
- Frusemide 1mg/kg PO q12hrs
- Benazepril 5mg PO q24hrs
- DIFFERENT - Use of Pimobendan (half dose to what would give dog) -> off-label - ONLY if refractory to high doses of frusemide
- Owner to monitor respiration rate when Hamish is sleeping in a cool place
- Recheck at referring vets in 7 days to monitor response to treatment and check urea/creatinine/potassium/PCV/TP
85
Cat with HCM without congestive heart failure treatment what is the goal and how to achieve
- Reduce contractility - less mitral regurgitation
| ○ Beta blocker - atenolol - GIVEN PRIOR TO FAILURE IN HCM
86
Cat - restrictive cardiomyopathy medications and why
- Frusemide 1mg/kg PO q12hrs
- Spironolactone 1.5mg/kg PO q12hrs - can start early or later in the disease
- Benazepril 5mg PO q12hrs
- Clopidogrel 18.75mg PO q12hrs - acts on the platelets to stop aggregation to stop thrombus formation
- Pimobendan? 1.25mg PO q12hrs - may worsen if outflow obstruction - poor diastolic function may increase - only if refractory to frusemide
87
Dog - supraventricular tachycardia with history of mitral valve disease causing CHF what is the goal of treatment and medications that lead to this
reduce HR WITHOUT reducing contractility
- In addition to frusemide, ACEi, pimobendan and spironolactone - to control congestive heart failure
- Digoxin (recheck trough serum level in 7 days) + diltiazem (calcium channel blocker - slow down of electricity activity through nodes - slow HR) 1mg/kg PO q8hrs - to control heart rate
88
What is digoxin, function and mainly used for
- Positive inotrope (weak)
- Alters baroreceptor sensitivity
- Slows heart rate (increases PSNS tone)
- May directly produce natriuresis/diuresis
- Main use SVT - supraventricular tachycardia (QRS complexes tall and narrow without p waves accompanying)
DVM 3 - 1
flashcards
Decks in class (33)
# Cards
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ECP 1100
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ECP 292
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ECP 3106
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ECP 4100
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ECP 5100
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ECP 669
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Dog and Cat 1100
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Dog and Cat 2101
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Dog and Cat 399
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Dogs and Cats 4112
-
Birds 198
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Birds 2101
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Bird 3101
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Horses 1100
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Horses 2101
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Horses 394
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Bird 426
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Horses 4103
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Cattle 1101
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Cattle 2103
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Cattle 3100
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Cattle 447
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Dog and Cat 5100
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Dogs and Cat 6101
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Dog and Cat 7101
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Horses 589
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Dog and Cat 8101
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Dog and Cat 9100
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Dog and Cat 10100
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Dog and Cat 1188
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Small Rum 1101
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Small Rum 2100
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Small Rum 339
