Circulatory Disorders of Ruminants

Question 1

Heart rate of a lactating dairy cow is?

Answer 1

RR 60-80

Question 2

Tachycardia - 6 causes

Answer 2

Centrally - Cortico-stimulation - catecholamine
Peripherally Increased demand (lactating, eating etc)
Decrease in blood volume
Severe anemia
Decreased cardiac function
Arrhythmia

Question 3

Bradycardia - 7 causes

Answer 3

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

Question 4

Heart rate or rhythm doesn’t fit it what do you do?

Answer 4

ECG

Question 5

Shock - name 7 types

Answer 5

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)

Question 6

Leptospirosis - 5 types

Answer 6

Aerobic motile spirochete

Hardjo (host adapted), pomona (non-host adapted), gryppotyphosa, itcterohemorrhagica, canicola

Question 7

Host adapted Lepto - causes what?

Answer 7

Repro problems, chronic persistent infections

Question 8

Non-host adapted Lepto - causes what?

Answer 8

acute infection in accidental hosts

Question 9

Epidemiology of Lepto

Answer 9

warm & wet
skin abrasions & mucus membranes
Urine, uterine fluids, spread venerially
After recovery can still shed

Question 10

Leptospirosis - pathogenesis

Answer 10

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

Question 11

Leptospirosis - acute

Answer 11

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

Question 12

Leptospirosis - sheep

Answer 12

rare, but often sudden death

Question 13

Leptospirosis - adult cattle

Answer 13

Usually hardjo

Question 14

Initial infection of Leptospirosis - adult

Answer 14

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

Question 15

Leptospirosis - diagnosis

Answer 15

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

Question 16

Leptospirosis - prevention

Answer 16

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

Question 17

Cold water hemoglobinurea

Answer 17

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

Question 18

Cold water hemoglobinurea - pathogenesis

Answer 18

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)

Question 19

Copper poisoning

Answer 19

Acute hemolysis because of chronic copper poisoning
Either primary (lot at once, or chronic) or secondary (plant, toxic)

Question 20

Copper poisoning - pathogenesis (acute/chronic)

Answer 20

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

Question 21

Copper poisoning - clinical signs

Answer 21

acute - GI issues, diarrhea, dysentary & jaundice, shock, abdominal pain
chronic- pale, jaundice, low appetite, tachycardia, depressed, tachypnea, maybe neurosigns later, anemia, methemoglobinemia, hypoxia & dyspnea

Question 22

Copper poisoning - clinical path

Answer 22

anemia, hemoglobinemia/urea, methemiglobinemia/urea

high copper, high liver enzymes

Question 23

Copper poisoning - treatment

Answer 23

don’t stress
give a chelator - molybdenum to get the copper out.
(if suspected)

Question 24

Copper poisoning - prevention

Answer 24

keep copper low in feed, or if you know about their molybdenum intake, you can give a little more

Question 25

Heart failure - right or left?

Answer 25

right

Question 26

Right-sided heart failure

Answer 26

Increase in heart right, decrease in appetite, exercise tolerance Ventral edema, jugular distension, jugular pulse, extremities cool, elbows abducted

Question 27

Left-sided heart failure - rare

Answer 27

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

Question 28

Treatment

Answer 28

poor prognosis, probably already permanent damange, could try diuretics

Question 29

Arrhythmias

Answer 29

Heart disease usually, supra ventricular dysrhythmias rare, but usually a/fib cattle do get normal sinus arrhythmia.

Question 30

Atrial Fibrillation

Answer 30

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)

Question 31

Endocarditis

Answer 31

Valvular or non-vavluar | A. pyogenes, e.coli or alpho-hemolytic strep

Question 32

Endocarditis - pathogenesis

Answer 32

Disturbed blood flow -> damage to endocardium -> platelet adhesion/fibrin clumps -> bacteria can colonize if circulating

Question 33

Endocarditis - Predisposing factors

Answer 33

valvular regurg/stenosis, heart disease, none

Question 34

Endocarditis - clinical finding

Answer 34

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

Question 35

Endocarditis - clinical pathology

Answer 35

neutrophilia (with or without left shift) anemia hyperfibrinogenima Hypergloblinimia

Question 36

Endocarditis - post mortem

Answer 36

vegetative growths that distort the valves Examine the chordae & the rest of the endocardium (hard to culture) Other lesions consistent with embolization & abscess

Question 37

Endocarditis - treatment

Answer 37

ideally culture first Start with broad spectrum Change to what culture says Continue for more than 14 days

Question 38

Cardiomyopathy - what kind is in bovine?

Answer 38

DCM Inherited - red gene in Holsteins Diffuse myocardial fibrosis association Clinical signs = right heart failure

Question 39

DCM - diagnosis

Answer 39

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

Question 40

Myocarditis

Answer 40

Bacterial - h. somni, a. pyogenes, clostridia | Viral - FMD, bluetongue

Question 41

Myocardial degeneration

Answer 41

Toxin (ionophore, bacterial toxemia, gosseypole) | Nutrition (vitamin e & selenium deficiency, excessive molybdenum or sulphates)

Question 42

Myocarditis/Myocardial degeneration

Answer 42

Sudden death Chronic - heart failure, arrhythmias Vitamin e/selenium -> die when exercised

Question 43

Myocarditis/Myocardial degeneration - clin path

Answer 43

Can look at CK Tropanin 1 Otherwise underlying cause

Question 44

Myocarditis/Myocardial degeneration - treatment

Answer 44

Remove/treat underlying cause Rest, decrease stress Anti-inflammatories in myocarditis Don't treat with anti-arrhytmias

Question 45

Myocarditis/Myocardial degeneration - PM

Answer 45

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

Question 46

Pericardial disease (TRP)

Answer 46

In ruminants usually, pericarditis (TRP in cows) Sheeps/goats/calves - sequelae of septicemia Hardware ingested, decreased everything, venous engorgement, elbows are abducted Undulating disease

Question 47

Friction rubs

Answer 47

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

Question 48

Triad of diagnostic clinical signs for pericardial disease

Answer 48

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

Question 49

Pericardial disease - treatment

Answer 49

antibiotics drain pericardial sac Remove FB by surgery

Question 50

Pericardial disease - sequelae

Answer 50

Fibrin --> fibrosis, constrictive pericarditis

Question 51

High mountain disease

Answer 51

``` Chronic heart failure in cows living in high altitude. Low atmospheric oxygen Alveolar hypoxia Pulmonary vasoconstriction/hypertension right heart failure Cor pulmonale ```

Question 52

High mountain disease - animals affected

Answer 52

Holsteins (tunica media is more sensitive) predisposed, sheep & goats pretty resistant introduced animals

Question 53

High mountain disease - pathogenesis

Answer 53

Low O2 Myocardial damage Need to slowly adapt them.

Question 54

High mountain disease - PM

Answer 54

CHF, concentric right ventricular hypertrophy

Question 55

Congenital heart disease

Answer 55

Variable incidence, can be simple or complex Simple - VSD ASD/PD are less common Complex - rare (tetraology of fallow), persistent truncus arteriosis etc)

Question 56

Congenital heart disease - Clinical significance

Answer 56

Consider the direction of the shunt | Possible extra-cardiac effect could alter cardiac function (e.g. pulmonary hypertension)

Question 57

Left-to-right shunts

Answer 57

Increase the workload of both the chambers (left more than right) Decrease the cardiovascular functional capacity Cause failure to thrive

Question 58

Right-to-left-shunt

Answer 58

similar to L-to-R, but even worse because of hypoxemia

Question 59

Congenital heart disease - Clinical signs

Answer 59

variable - from asymptomatic, to gradually progressive to severe/immediate (exercise intolerance) - resp distress (can do blood gasses, grave prognosis)

Question 60

Simple VSD

Answer 60

Loudest very forward on the right

Question 61

Complex VSD

Answer 61

Loudest on the left

Question 62

PDA in ruminants is simple or complex

Answer 62

Complex in ruminants