Heart rate of a lactating dairy cow is?
RR 60-80
Tachycardia - 6 causes
Centrally - Cortico-stimulation - catecholamine
Peripherally Increased demand (lactating, eating etc)
Decrease in blood volume
Severe anemia
Decreased cardiac function
Arrhythmia
Bradycardia - 7 causes
Hypoglycemia
Decrease in catecholamines
Conserve energy
Vagal stimulation
Hyper/Hypokalemia (if severe causing A/V block)
Increased intra-cranial pressure
Arterial pressure is less than the inter-cranial pressure
Heart rate or rhythm doesn’t fit it what do you do?
ECG
Shock - name 7 types
Hypo-perfusion
Cardiogenic
Hypo-volemic
Toxic (micovascular failure)
Endotoxic (bacterial toxins on the heart)
Septic (septicaemia with affect on organs & vasculature)
Neurogenic (intense stimulus - emotions, vagal, CNS trauma)
Leptospirosis - 5 types
Aerobic motile spirochete
Hardjo (host adapted), pomona (non-host adapted), gryppotyphosa, itcterohemorrhagica, canicola
Host adapted Lepto - causes what?
Repro problems, chronic persistent infections
Non-host adapted Lepto - causes what?
acute infection in accidental hosts
Epidemiology of Lepto
warm & wet
skin abrasions & mucus membranes
Urine, uterine fluids, spread venerially
After recovery can still shed
Leptospirosis - pathogenesis
Enters abrasion
Multiplies in blood
Liver/spleen brain
blood vessels/liver damage
Proximal tubules of kidneys/placenta/fetus damage
Recover? antibodies remove everything but eye, uterus & renal system
Leptospirosis - acute
calves < 1 month
high mortality (sudden death)
pyrexia, depression, anorexia, petichea, acute hemolytic anemia, hemoglobinurea, super anemic, tachycardic, have shock
(usually caused by pomona)
direct damage to the micro-circulation - blood loss - tachycardia, less O2 carrying –> tachycardia, peripheral vasoconstriction –> edema (damaged blood vessels, hypoxia, cell death, tachypnea & dyspnea
Leptospirosis - sheep
rare, but often sudden death
Leptospirosis - adult cattle
Usually hardjo
Initial infection of Leptospirosis - adult
pyrexia, anarexia, agalactia & stiffness
Recnet in intro? mastitis Agalactia, abortions a few weeks later
Sequelae - persists in repro tract, infertility (fetal infection, but also placentitis) & transmitted venereally
Mastitis - without gland inflammation - possible
Leptospirosis - diagnosis
Culture, but only do this in acute cases (pomona)
Dark field microscopy
PCR - don’t tell you the serovar
Serology - can look at a rising titre, but hard to know if the herd is endemic
Leptospirosis - prevention
vaccine - server specific
reduces shedding as well
Can do as young as 4 weeks, repeat every 6-12 months, doesn’t prevent abortions or renal shedding
Control - hard to identify carriers, can try to control shedding & spreading & have good hygiene
Cold water hemoglobinurea
Happens when you drink a whole lot of cold water - intravascular hemolysis - usually in calves (rumen is buffer). Usually after a period of water deprivation
Cold water hemoglobinurea - pathogenesis
Absorb water, decreases, blood electrolytes, decreases osmotic pressure,
RBC are the most fragile at 5 months
occurs within 1 hour of ingestion
tachycardia due to relative O2 deprivation
cell death, vasodilation, edema (pulmonary, brain, death)
Copper poisoning
Acute hemolysis because of chronic copper poisoning Either primary (lot at once, or chronic) or secondary (plant, toxic)
Copper poisoning - pathogenesis (acute/chronic)
Acute - actual chemical damage to the GI mucosa, causing protein to coagulate causing coagulation necrosis, fluid loss, shock & death
Chronic - poorly understood - no clinical signs until critical levels in liver, liver necrosis - releases copper, oxidizes blood cells, methemoglobinemia, heinz bodies, hemolysis
PCV can decrease in 48 hours seriously
Copper poisoning - clinical signs
acute - GI issues, diarrhea, dysentary & jaundice, shock, abdominal pain
chronic- pale, jaundice, low appetite, tachycardia, depressed, tachypnea, maybe neurosigns later, anemia, methemoglobinemia, hypoxia & dyspnea
Copper poisoning - clinical path
anemia, hemoglobinemia/urea, methemiglobinemia/urea
high copper, high liver enzymes
Copper poisoning - treatment
don’t stress
give a chelator - molybdenum to get the copper out.
(if suspected)
Copper poisoning - prevention
keep copper low in feed, or if you know about their molybdenum intake, you can give a little more
Heart failure - right or left?
right
Right-sided heart failure
Increase in heart right, decrease in appetite, exercise tolerance
Ventral edema, jugular distension, jugular pulse, extremities cool, elbows abducted
Left-sided heart failure - rare
Tachycardia, etc similar to right
Increase in pulmonary pressure, probably won’t have many respiratory signs, unless pulmonary edema (frothing at the nares etc)
First sign - might be right sided heart failure
Treatment
poor prognosis, probably already permanent damange, could try diuretics
Arrhythmias
Heart disease usually, supra ventricular dysrhythmias rare, but usually a/fib cattle do get normal sinus arrhythmia.
Atrial Fibrillation
Lose coordinated electrical activity of the atria (sometimes you get AV node ventricular activity)
On ECG, no p-waves, irregular base line (as in f waves) undulating baseline… every once in a while, normal random QRS
Occurs especially with atrial enlargement
Can occur spontaneously with sub-acute or chronic GI disease
If persistent, heart disease or heart failure
Always clinically relevant (toxemia, severe electrolyte imbalances, myocardial abnormalities)
Endocarditis
Valvular or non-vavluar
A. pyogenes, e.coli or alpho-hemolytic strep
Endocarditis - pathogenesis
Disturbed blood flow -> damage to endocardium -> platelet adhesion/fibrin clumps -> bacteria can colonize if circulating
Endocarditis - Predisposing factors
valvular regurg/stenosis, heart disease, none
Endocarditis - clinical finding
poor doing weight loss, shifting lamens associated with arthritis, fluctuating fever goes away with antibiotics, may or may not have a heart murmur
Usually tricuspid on the atrial surface
Lungs showered, will get cough
Lots of these? pulmonary hypertension, after load increases, right volume overload
Left - renal/myocardial infarcts, maybe septic arthritis
Endocarditis - clinical pathology
neutrophilia (with or without left shift)
anemia
hyperfibrinogenima
Hypergloblinimia
Endocarditis - post mortem
vegetative growths that distort the valves
Examine the chordae & the rest of the endocardium (hard to culture)
Other lesions consistent with embolization & abscess
Endocarditis - treatment
ideally culture first
Start with broad spectrum
Change to what culture says
Continue for more than 14 days
Cardiomyopathy - what kind is in bovine?
DCM
Inherited - red gene in Holsteins
Diffuse myocardial fibrosis association
Clinical signs = right heart failure
DCM - diagnosis
R/O other causes of right heart failure
See the clinical signs like this in an otherwise healthy animal
Congestive heart failure and extensive myocardial fibrosis
Myocarditis
Bacterial - h. somni, a. pyogenes, clostridia
Viral - FMD, bluetongue
Myocardial degeneration
Toxin (ionophore, bacterial toxemia, gosseypole)
Nutrition (vitamin e & selenium deficiency, excessive molybdenum or sulphates)
Myocarditis/Myocardial degeneration
Sudden death
Chronic - heart failure, arrhythmias
Vitamin e/selenium -> die when exercised
Myocarditis/Myocardial degeneration - clin path
Can look at CK
Tropanin 1
Otherwise underlying cause
Myocarditis/Myocardial degeneration - treatment
Remove/treat underlying cause
Rest, decrease stress
Anti-inflammatories in myocarditis
Don’t treat with anti-arrhytmias
Myocarditis/Myocardial degeneration - PM
don’t see much histo
Can see a streatked pallor on the myocardium if vitamin/E/selenium
Myocarditis abscess - may see these, patchy though, not diffuse
Pericardial disease (TRP)
In ruminants usually, pericarditis (TRP in cows)
Sheeps/goats/calves - sequelae of septicemia
Hardware ingested, decreased everything, venous engorgement, elbows are abducted
Undulating disease
Friction rubs
Important to differentiate from a murmur. These can vary from beat-to-beat and in timing with relation to the beats. (both character & intensity)
Can disappear with the appearance of effusion
Triad of diagnostic clinical signs for pericardial disease
Muffled heart sounds
Weak rapid pulse
Venous engorgement
(Can do U/S, ECG, large & small alternating QRSs, pericardio-centesis)
Can see fibrin, thickened pericardium, purulence, may see FB. Reticulum communication possible
Pericardial disease - treatment
antibiotics
drain pericardial sac
Remove FB by surgery
Pericardial disease - sequelae
Fibrin –> fibrosis, constrictive pericarditis
High mountain disease
Chronic heart failure in cows living in high altitude. Low atmospheric oxygen Alveolar hypoxia Pulmonary vasoconstriction/hypertension right heart failure Cor pulmonale
High mountain disease - animals affected
Holsteins (tunica media is more sensitive) predisposed, sheep & goats pretty resistant
introduced animals
High mountain disease - pathogenesis
Low O2
Myocardial damage
Need to slowly adapt them.
High mountain disease - PM
CHF, concentric right ventricular hypertrophy
Congenital heart disease
Variable incidence, can be simple or complex
Simple - VSD
ASD/PD are less common
Complex - rare (tetraology of fallow), persistent truncus arteriosis etc)
Congenital heart disease - Clinical significance
Consider the direction of the shunt
Possible extra-cardiac effect could alter cardiac function (e.g. pulmonary hypertension)
Left-to-right shunts
Increase the workload of both the chambers (left more than right)
Decrease the cardiovascular functional capacity
Cause failure to thrive
Right-to-left-shunt
similar to L-to-R, but even worse because of hypoxemia
Congenital heart disease - Clinical signs
variable - from asymptomatic, to gradually progressive to severe/immediate (exercise intolerance) - resp distress
(can do blood gasses, grave prognosis)
Simple VSD
Loudest very forward on the right
Complex VSD
Loudest on the left
PDA in ruminants is simple or complex
Complex in ruminants