Rotations Flashcards
Hypotention what to do in that situation
a. Check patient depth -> deep then decrease inhalant and reassess
b. Check HR -> low then administer anticholinergic (glycopyrrolate – 5-20mcg/kg, 40-60mins)
c. Normal HR –> crystalloid bolus (up to 30ml/kg – so up to 3 bolus of 10ml/kg)
d. Fluid not working but HR still good
o Vascular tone + ionotropic support – ephedrine (0.1mg/kg, lasts 10-15mins) – can give x2
o Dopamine CRI – 7-10mcg/kg/min -> (beta agonist – positive inotrope, alpha agonist – vasoconstriction – middle to large doses)
o Dobutamine (ionotropic support), Vasopressin (increase vascular tone – vasoconstricts gut so can get sloughing – diarrhoea) - BIG GUNS
Reasons for hypotention
- hypothermia, too deep anaesthesia, vasodilating drugs (iso, ace), bradycardia, reduced contractility of the heart
reasons for hypertension
- too light anaesthetic, pain, kidney disease, hyperthyroid, vasoconstrictive drugs (alpha-2), fluid overload
what drug is atropine, effects, how long lasts and side effects
anti-cholinergic - increase HR and BP
lasts 10-15mins
side effects - SLUD - salivation, lacrimation, urination, defecation, and ventricular tachycardia
what are some reasons for pale MM
- decreased oxygen carrying capacity of the blood, bleeding/shock, reduced oxygen availability, pain, alpha-2 agonist
bradycardia during anesthesia what level, how to respond
(HR < 50-70 dog, <100 cat)
-Only issue if low BP or an escape rhythm (no P waves)
– give anticholinergic (ensure not hypothermic)
Hypercapnia at what level and how to respond
CO2 >60mmHg
a. Hypoventilation – provide IPPV or mechanical ventilation and reassess depth
b. Rebreathing CO2 – non-rebreathing low fresh gas flow, rebreathing – exhausted soda lime
which LN can you normally feel
popliteal, sub-mandibular, pre-scapular
Thrombocytopaenia what levels normal, risk of bleeding and spontaneous bleed, clinical signs and immune-mediated what need to do first
normal 200-500, risk of bleeding <50, spontaneous bleeding <30
- Will bruise easily, petechiae -> ear, gums, ventral obstruction, vulva, gastrointestinal (melena), eyes and brain (more serious but rare)
Immune mediated thrombocytopaenia - primary or secondary (drug - penicillin, cephalosporins, inflammatory, infectious, neoplasia (lymphoma)
- Need to evaluate as to whether secondary even though primary more common
maropitant what type of drug and effects
- neurokinin-1 (NK-1) receptor antagonist that acts in the CNS by inhibiting the binding of substance P, which is the key neurotransmitter involved in vomiting.
- can suppress both peripheral and centrally mediated emesis.
- has been shown to reduce the minimum alveolar concentration (MAC) requirements of sevoflurane and to reduce visceral pain in dogs, as NK-1 receptors are stimulated by substance P
- has been shown to possess anti-inflammatory activity
Mirtazapine whaa is it and effects
- Tetracyclic Antidepressant; 5-HT3 Antagonist
- appetite stimulant and anti-emetic with chronic kidney disease
- possible anti-depressant activity with sedative effects
Omeprazole what type of drug and effects
Proton pump inhibitor
- treatment and prevention of ulcers
What is RER, equation and how to determine DER
- RER (kcal/day) = 30 x BW (kg) + 70
- RER (kcal/day) = 70 x BW (kg)0.75 (dogs > 45 kg) - based on ideal body weight
- DER = RER x “lifestyle factor”
1. Determine ideal weight (BCS)
2. Calculate RER
3. Determine lifestyle factor to calculate DER
What levels of fat and protein needed for 1) diabetic cat 2) cat with advanced renal disease 3) schauzer with hypertriglyceridaemia
Diabetic cat -> normal fat and high protein
Cat with advanced renal disease -> high fat low protein
Schnauzer with hypertriglyceridemia -> low fat and normal protein
Toxicity of gentamicin
Nephrotoxicity and ototoxicity (cranial nerve 8 - if tympanic membrane is ruptured DON’T USE)
Single large doses have been shown to reduce nephrotoxicity
Toxicity of enroflocaxin
Cartilage breakdown in juveniles, blindness in cats (dose related) - DON’T USE IN CAT AND JUVEINILES
- Single large dose better for preventing resistance
Toxicity of tetracyclines
Degradation products cause nephrotoxicity (ototoxicity) and hepatotoxicity and photosensitivity (if use in cattle give shade)
what antibiotics don’t use in horses and rabbits and why
Erythromycin Clindamycin Lincomycin Metronidazole GIT ISSUES
abnormalities where is the lesion - forced expiration and inspiratory dyspnoea
1) Forced expiration (most of the time increase in inspiratory effort)
- Small airway disease (Asthma)
- Fixed upper airway obstruction (will also see inspiratory)
2) Inspiratory dyspnoea (short expiration)
- Upper airway obstruction (Stertor or stridor) - more common
- Severe, chronic pleural effusion (no noise)
abnormalities where is the lesion - paradoxical abdominal movement
2) Paradoxical abdominal movement - more severe dyspnoea
- Upper airway obstruction
- Stiff lungs - less compliant
- Diaphragm dysfunction
- Severe chronic pleural effusion in cats (usually fluid)
abnormalities where is the lesion - inspiratory dyspnoea with an expiratory pish and short shallow respiratory
4) Inspiratory dyspnoea with an expiratory push
- Fixed upper airway obstruction (cannot be pushed away)
5) Short shallow respiratory
- Some pleural space lesions
- Others as well
what are signs of severe dyspnea and critical
Signs of severe dyspnoea - Extended neck - Abducted elbows - Open mouth breathing - Anxious facial expression (how distressed is the animal? - chronic may be less stressed) Critical - Lateral recumbency - Pupillary dilation - RESPIRATORY ARREST - Cyanosis if caused by hypoxia - OXYGEN
Thoracocentesis how perform
(8th intercostal space)
□ Cranial to rib, ventral (4o’clock) for fluid, dorsal (2o’clock) for air
□ Sterile gloves, hyperdermic needle, 3 way-tap, EDTA tube
□ Go in bevel up at 90 degrees and keep moving slowly forward until no more negative pressure, once no negative pressure then can redirect the needle (NOT BEFORE this as can tear the pleura)
pulmonary parenchymal disease clinical signs and causes
crackles, short shallow breathes as it gets worse than deep breaths, paradoxical
○ Causes
§ Neoplasia, pneumonia, PTE, oedema
□ Cardiogenic oedema
® What results - get increase in hydrostatic pressure resulting in water overload - once reduce water with diuretics (such as frusemide) then normal mechanisms take over (pneumocytes)
□ Non-cardiogenic oedema
® Upper Respiratory Obstruction
◊ Large inspiration against closed glottis, large -ve pressure build up
® Neurogenic (electrocution)
◊ Large increase in sympathetic tone results in large amount of blood flow into the lungs
® What results -
◊ Capillary rupture -> not just water within the oedema also cell debris and protein
Cardiac tamponade what occurs and how generally presents
(compression/collapse) -> increase pressure will affect the right side of the heart first (thinner wall as moving blood into lower pressure system) -> increase pressure into the vena cava (abdominal effusion) -> decrease filling during diastole -> decrease SV -> short and narrow pulses
Common presentation - Muffled heart sounds, short and narrow pulses, large breed dog, ultrasound to confirm
arterial blood gas what PaO2 levels that are bad, how to determine issue, what look with glucose and lactate
- PaO2 = oxygenation
○ <75 needs oxygen
○ <55 life-threatening - Determining acid-base
1. Look at the pH -> acidosis or alkalosis?
2. Look at what is causing that change
§ PaCO2 - if HIGH then RESPIRATORY ACIDOSIS - correlates or compensatory mechanism
§ SBE (standard base excess - amount of base to add to get normal pH (7.4) - if NEGATIVE then not much base so METABOLIC ACIDOSIS
3. Is there a compensatory mechanism - should always be one at about 1:1 - Glucose - very high suggests diabetes OR close to death (massive corticosteroid release which results in insulin resistance)
- Lactate - high - reduced perfusion
What are the 4 main causes of metabolic acidosis
- Phosphorus and sulphates (azotaemia) - not being urinated out
- Lactic acidosis
- Ketone acidosis
- Toxic - 1080, ethylene glycol
what are the 3 main measures of perfusion
1) Lactate - high
2) Venous CO2 (if low could be hypoperfusion or hyperventilation (check RR))
3) Blood pressure - direct measure - hypovolaemia
what is the difference between hypovolaemic and cardiogenic shock and why important
NEED TO KNOW - one gets fluids and one gets beta blockers
- U/S heart
○ in cardiogenic cannot contract with large blood volumes within the ventricle
○ In hypovolaemic shock the contractility is fine just don’t have the volume
Beta 1 and 2 receptors what do they do
- Beta 1 - lusitropy (increase relaxation of myocardium to allow for filling), contractility, chronotropy (increase heart rate)
○ DCM - agonist - debutamine - Beta 2 - vasodilation, bronchodilation - lower airway disease
radiographs what vertebrae for underinflated vs well-inflated
-Underinflated lungs – cura intersect vertebrae T9
-Well-inflated lungs – cura intersect vertebrae at T12/13
o Lung pathology easiest to see if surrounded by well-aerated lung
Cardiomegaly what are the rules for dog radiographs - lateral (3) and VD (!)
Lateral
1. Size of the heart - Two thirds height of thorax from base to apex (yellow line)
2. Cranial to caudal margin of heart -> 2.5-3.5 intercoastal spaces wide
3. Trachea should deviate from thoracic spine at about 40degrees (blue)
VD -
1. heart should be 2/3rds the width of the thorax
Cardiomegaly what are the rules with radiographs forr cats, lateral
Lateral
1. 5th - 7th rib rule
• Work out distance between cranial boarder of 5th rib and caudal boarder of 7th and the heart shouldn’t be greater than that distance from cranial to caudal
General changes with cardiomegaly seen radio-graphically
– elevation of trachea, increased craniocaudal diameter of the heart (Width), increased sternal contact, valentine shaped heart (cat) – left atrium sits more cranial than in dogs
General changes with right-sided enlargement and left side enlargement of heart radiographically
- Right sided enlargement – cranial bulging of right heart border
- Left sided enlargement – expansion of left atrium caudal lobar area (left atrial wedge), straightening of the caudal boundary (left ventricle enlargement), bulge at 2-3 o’clock on VD (left auricle enlargement)
what are the most common congenital and acquired cardiac diseases for dogs and cats
Dogs
• Congenital - PDA (patent ductus arteriosus), pulmonic or subaortic stenosis, mitral or tricuspid valve dysplasia, persistent right aortic arch
• Acquired – DCM (dilated cardiomyopathy), ARVC (arrhythmogenic right ventricular cardiomyopathy (boxer),
Cats
• Congenital – tricuspid or mitral valve dysplasia, atrial septal defect (ASD), ventricular septal defect
• Acquired – hypertrophic cardiomyopathy, restrictive cardiomyopathy
Pulmonary vasculature on radiographs where located in respect to each other and what are the VD (2) and Lateral (1) rules
Lateral – look for pairs - Dorsal to ventral – artery, bronchus, vein
VD – veins are central to arteries
Look at vessels when cross the 9th rib
VD
1. Can be 1.2 times width of the 9th rib when cross the rib
2. The artery and vein should be the same width
Lateral
• Proximal portion of the 4th rib of the 4th intercostal space-> harder to do
Causes of enlarged pulmonary veins, enlarged arteries, both enlarged and small vessels
- Enlarged veins - Mitral insufficiency, volume overload, patent ductus arteriosus, primary myocardial disease, left atrial obstruction (neoplasia, thrombosis)
- Enlarged arteries (not as common) – parasitic arteritis (heartworm disease), thromboembolic disease, chronic lung disease with pulmonary hypertension
- BOTH enlarged – iatrogenic fluid overload, left to right shunting, fluid retention, peripheral arterio-venous fistula
- Small vessels – hypovolaemia, right to left shunting, severe pulmonary stenosis
Causes of alveolar vs bronchial pulmonary patterns
Alveolar - • Aspiration pneumonia, cardiogenic and non-cardiogenic oedema
Bronchial - • Feline asthma, bronchopneumonia, age related change, chronic inflammation, idiopathic fibrosis, lungworm, neoplasia (lymphoma, bronchogenic carcinoma) – confirm via BAL
Differentials for lesions in cranioventral lungs, caudodorsal, diffuse, focal and multifocal lesions
Cranioventral – aspiration pneumonia (Alveolar pattern), all pneumonia, haemorrhage, neoplasia and bronchitis
Caudodorsal – cardiogenic pulmonary oedema (dog most common), non-cardiogenic pulmonary oedema (upper airway obstruction, head trauma), haemorrhage, pneumonia, neoplasia, bronchitis and fibrosis
Diffuse – cardiogenic pulmonary oedema, haemorrhage, pneumonia, neoplasia, bronchitis, fibrosis
Focal – solitary masses – CHANG
• C – cyst, H – haemotoma, A – abscess, N – neoplasia, G – granuloma
Multifocal – pulmonary metastases (need to be greater than 0.5-1cm in diameter), granulomatous disease, haemorrhage