Cardio Flashcards

1
Q

the three types of injectable selenium supplement in order of greatest selenium content

A

Mu-Se (5 mg/mL) -
labeled for weanling calves and mid-gestation beef cows

E-Se (2.5 mg/mL) - labeled for horses

Bo-Se (1 mg/mL) - labeled for calves, lambs, ewes, sows, piglets

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2
Q

differentials/mechanisms for ascites

A
heart failure (septal defect, valve failure, endocarditis, pericarditis, traumatic reticulo-pericarditis) with backup into Caudal vena cava -> leakage into abdomen. 
Liver dysfunction -> low oncotic pressure. 
May not be true ascites - hydrops,
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3
Q

differentials for muffled heart sounds

A
Pneumonia, plueropneumonia. 
pericardial effusion. 
pleural effusion. 
diaphragmatic hernia. 
abscess, mass, or air in mediastinum. 
pneumothorax. emphysema. 
fat.
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4
Q

typical signs/manifestations of CV disease

A
Edema, pleural effusion, ascites. 
Arrhythmias. 
Murmurs. 
Muffled heart sounds. 
exercise intolerance, weakness.
syncope (fainting)
Venous distension +/- pulsation. 
Painful peripheral swelling.
Lymphadenomegaly.
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5
Q

Mechanisms of edema, and which are the most common in ruminants?

A

increased vascular permeability.
increased hydrostatic pressure in the vasculature
decreased oncotic pressure in vasculature
edema of lymph drainage.
increased oncotic pressure (doesn’t cause problems often)

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6
Q

signs that edema may be due to increased vascular permeability

A

Evidence of systemic inflammation/infection -

PE: pale MM, injected MM/sclera, petechiation, fever, tachycardia, tachypnea or dyspnea,

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7
Q

signs that edema may be due to increased hydrostatic pressure

A

venous distension/pulsation, tachycardia (if decreased cardiac output), murmur, arrhythmia, ascites, distal limb edema, …
DfDx: CHF, Tricuspid (RAV) valve insufficiency, Venous thrombosis, liver dz, portal v. obstruction…

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8
Q

edema due to decreased oncotic pressure occurs when:

Total Protein is below ___ and albumin is below ___

A

TP <5g/dL

albumin < 1.5 g/dL

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9
Q

three ways to get hypoproteinemia/hypoalbuminemia?

A

Don’t make it: starvation/inadequate protein in diet, liver dz
Lose it:
protein losing enteropathy, PL nephropathy, 3rd space loss (e.g. burns, uncommonly seen)
YOU screwed up (iatrogenic):
hemodilution

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10
Q

differentials for causes of lymphedema

A

tumor obstructing a lymph vessel or node.
trauma - damage to lymph vessels?
increased central venous pressure.

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11
Q

benign arrhythmias (sinus arrhythmia, sinus bradycardia) are typically due to ___

A

decreased feed intake/anorexia –> hypocalcemia!

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12
Q

pathologic arrhythmias most commonly seen in ruminants?

A

Atrial fibrillation, premature depolarization

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13
Q

pathologic arrhythmias are typically secondary to ___

A

GIT disease –> electrolyte disturbance, acid-base imbalance

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14
Q

the best way to treat pathologic arrhythmias in ruminants?

A

correct the electorlyte/acid base abnormality, usually the arrhythmia will resolve.

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15
Q

AV blocks occur when there is a delay between ___ & ___.

A

p wave & QRS complex

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16
Q

what are the types of AV block?

A

1st degree: increased time between P wave and QRS (prolonged P-R interval)
2nd degree: prolonged P-R interval with occasional dropped beats (2 normal for every 1 dropped?)
3rd degree: prolonged P-R interval with fewer than 2 beats for every dropped beat.

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17
Q

atrial standstill ECG findings?

A

NO P waves!

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18
Q

atrial standstill most commonly seen in what signalment and disorder?

A

calves with metabolic acidosis.

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19
Q

describe what happens to potassium during metabolic acidosis

A

the H+ gradient between intracellular and extracellular compartments gets messed up, causes K+ to move out of the cells –> hyperkalemia

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20
Q

describe the pathophysiology of atrial standstill

A

hyperkalemia -> myocardium membrane depolarization -> Opens Na+ channels, they become inactivated -> hyperkalemia causes repeated depolarization, but the Na+ channels have not been able to reset themselves (membrane repolarizaiton not taking place) -> cells are refractory to the depolarization signal -> atrial standstill –> can quickly progress to V-fib , asystole, and death

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21
Q

treatment for hyperkalemia/atrial standstill?

A

you need to do something FAST - Ca2+ IV is the best way to quickly treat these animals –> causes the membrane depolarization threshold to shift so that the electical conductivity of the heart can go back to normal. THEN you need to fix the hyperkalemia - bicarbonate will re-establish the acid balance, drive K+ back into cells. Insulin will also work.

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22
Q

causes of arrhythmias in ruminants

A
electrolyte abnormalities. 
pericarditis. 
valvular disease. 
myocardial disease. 
toxemia. 
Cor Pulmonale. 
Lymphosarcoma. 
Fever.
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23
Q

Reynolds’ number is calculated by the ratio of ___ to ___

A

velocity: viscosity

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24
Q

turbulence of blood flow occurs when Reynolds’ number is greater than

A

2000

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25
Q

animals are predisposed to murmurs if there is an (increase or decrease?) in velocity or (increase or decrease?) in viscosity of blood?

A

increased velocity

decreased viscosity

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26
Q

typically, murmurs can be heard after PCV falls below ___

A

25% (but not all animals with PCV<25 have a murmur)

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27
Q
PMI for murmurs: 
Pulmonic valve
Aortic valve
Mitral (LAV) valve
Tricuspid (RAV) valve
A

PV: left, basilar, 3-4th ICS
AoV: left, basilar, 4-5th ICS, radiates up aorta
MV: left, apical, 5-6th ICS (near elbow)
TV: right, apical, 3-4th ICS (between shoulder & elbow)

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28
Q

systolic ejection murmur occurs between which heart sounds? describe the sound.

A

S1 & S2

increases in volume and then decreases <>

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29
Q

Holosystolic regurgitation murmur occurs between which heart sounds? describe the sound

A

S1 & S2

flat sound, same volume throughout systole.

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30
Q

diastolic decrescendo murmur occurs during which heart sounds? describe the sound

A

S4 & S1, S2 & S3

starts loud and then volume decreases

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31
Q

causes of ejection murmurs

A

innocent murmur (no clinical signs or lesion associated)
anemia, fever
Aortic or Pulmonic valve stenosis
Atrial or Ventricular Septal Defect, Tetrology of Fallot

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32
Q

causes of regurgitant murmurs

A

Mitral or Tricuspid valve insufficiency (regurg)

VSD, tetrology of Fallot

33
Q

normal jugular pulse/distension may be seen in what portion of the neck / how far away from the base of the heart (with animal’s head up)

A

caudal 1/3 of neck / about a hands-breadth from the base of the heart.

34
Q

mechanism of jugular distension/pulsation

A

decreased right ventricular filling (there is an increase in resistance to filling)

35
Q

typical causes of jugular distension/pulsation

A

RH failure
constrictive pericarditis
cardiomyopathy

If prominent pulsations:
Tricuspid regurg
Arrhythmia assoc. w/ atrial contraction against a closed AV valve

36
Q

most common reported congenital disease

A

Ventricular septal defect

37
Q

describe VSD murmur

A

Bilateral, harsh, plateau, pansystolic.
PMI: Right apex (tricuspid area) initially, because L to R shunt > left base (pulmonic area) later
palpable thrill

38
Q

what is Eisenmenger’s complex?

A

L -> R shunt is converted to a R-> L shunt d/t increased pressure in pulmonary artery and results in reversal of blood flow, severe hypoxia, pulmonary hypertension.
https://emedicine.medscape.com/article/154555-overview

39
Q

describe the ductus arteriosis in a normal calf

A

Ductus arteriosis should close prior to birth in calves (foals - closes within 96 hr of birth). DA is closed d/t decreased pulmonary vascular resistance and increased systemic vascular resistance.

40
Q

describe the murmur associated with PDA

A

continuous, high pitched, “machinery”
PMI: lounder on left, audible on both sides, 3-4th ICS
May be no murmur if large hole.

41
Q

what are the defects involved with tetrology of fallot?

A

Overriding aorta,
VSD,
RV hypertrophy,
obstruction of pulmonary artery flow.

42
Q

describe murmur of tetrology of fallot

A

loud pansystolic murmur with thrill, Left 3-4th ICS.

43
Q

common presentation of Tetrology of Fallot?

A

Cyanotic calf/lamb/kid

44
Q

major rule-outs for tetrology of fallot?

A
respiratory distress (TF has murmur)
CNS distress (TF has no neuro issues)
45
Q

pathologic effects of tetrology of fallot?

A

VSD: ventricular shunting of blood (L –> R),
partial stenosis of pulmonary artery and pulmonic valve,
increased outflow from aorta,
RV hypertrophy

46
Q

atrial septal defect is commonly associated with which other congenital defect?

A

PDA

47
Q

describe the murmur associated with ASD

A

holosystolic ejection murmur, L heart base

48
Q

ASD shunt is typically which direction?

A

L–> R

49
Q

T/F? ASD murmur is always pathologic

A

False. may be innocent, calves are frequently asymptomatic

50
Q

other congenital heart defects seen in ruminants?

A
Pulmonic stenosis
Tricuspid atresia
Mitral chordae rupture
Ventricular hypoplasia
Truncus or pseudotruncus arteriosus
Aortic anomalies
Ectopia chordis cervicallis (heart outside of the thoracic inlet, in neck)
51
Q

Etiologies of Acquired Valvular diseases are typically __? (4)

A

degeneration, infection/inflammation, trauma, or unknown

52
Q

describe the murmur associated with acquired valvular diseases

A

systolic, regurgitant, left apex (5-6th ICS) if mitral, right apex (3-4th ICS) if tricuspid

53
Q

Valvular disease may occur secondary to chronic active infections such as ____ (at least 3 you should think of)

A

footrot
abscesses
rumenitis
other septic processes

54
Q

Common bacteria that cause valvular disease

A

Trueparella pyogenes, Strep. spp.

55
Q

Neoplastic process that may (rarely) cause valvular disease

A

lymphosarcoma (HULA - heart, uterus, lymph nodes, abomasal wall)

56
Q

how can you determine if a murmur is occurring between S1 & S2 (lub-sh-dup), or S2 & S1 (lub-dup-sh-lub-dup)?

A

palpate the carpal pulse while asculting –> if weak pulses then it is systolic murmur (i think?)

57
Q

prognosis for valvular disease

A

depends on etiology, onset, duration, severity; generally guarded to poor

58
Q

treatment for bacterial endocarditis

A

long term cidal abx (culture & sensitivity), aspirin, low-dose heparin, furosemide, digoxin

59
Q

what is cor pulmonale

A

aka brisket disease, pulmonary hypertension, high mountain disease.
Def: Heart disease secondary to lung dysfunction

60
Q

pathophys of cor pulmonale

A

Lung Dysfunction 2’ to [Low O2 tension/high altitude, BRD, lungworm, other infection, or toxins (locoweed)] –>
hypoxia –>
vasoconstriction of pulonary arterioles –>
Pulmonary hypertension –>
RV hypertrophy –>
RV dilation –> RV failure

61
Q

signs of cor pulmonale

A
brisket edema
jug distension/pulse
dyspnea, tachypnea
tachycardia
split S2 sound (Ao and Pul valves closing at different times)
Tricuspid or Pul valve insufficiency
62
Q

rule outs for cor pulmonale

A
endocarditis
CHF
cardiomyopathy
cardiac neoplasia (LSA)
pericarditis
pleuritis
pleural effusion etc
63
Q

in addition to cor pulmonale, what other heart pathology may occur with locoweed poisoning?

A

myocardial damage

64
Q

treatment for cor pulmonale

A

move to lower elevation
treat whatever primary lung disease is occurring, if any
diuretics, digoxin.
Px guarded if showing signs of RH fail.

65
Q

prevention of cor pulmonale

A

genetic selection: bulls with good Pulmonary Arterial Pressures at >5000 ft
remove susceptible cattle from herd (if altitude related)
prevent locoweed ingestion
vaccinate for BRD complex, prevent pulmonary dz

66
Q

myocarditis typically caused by ___?

A

infectious agents:
bacteria (S. aureus, C. chauvoei, Mycobacterium spp.)
viruses (FMD)
parasites (strongyles, toxoplasma, sarcocysts, Borrelia [Lyme])

67
Q

what’s the difference between myocarditis and cardiomyopathy?

A
Myocarditis = inflammation of mycardium (typically caused by infectious agents)
Cardiomyopathy = subacute/chronic dz of ventricular myocardium, WITHOUT dz of valves, vessels, or lungs.
68
Q

Causes of cardiomyopathy

A

inherited (red holsteins, polled Herefords)
toxins (monensin, lasalocid, gossypol, Phalaris grass.
** Most common etiology: Mineral imbalances (Cu, Se deficiency; Mo, sulfates high)
lymphosarcoma

69
Q

treatment of cardiomyopathy, myocarditis

A

treat underlying dz
supportive care
may be too late/guarded Px

70
Q

definition of pericarditis

A

inflammation or pericardium resultiing in accumulation of fluid/exudate between visceral and parietal pericardium

71
Q

etiologies of pericarditis

A

trauma (most common) TRP
hematogenous
extension from lungs or pleura
neoplasia

72
Q

Hallmark signs of pericarditis

A

Muffled heart sounds
Pericardial friction rub “washing machine murmur”
Signs of RH fail

73
Q

treatment for pericarditis

A

usually salvage, poor Px: drainage (pericardectomy), 5th rib resection

74
Q

prevention of pericarditis

A

magnets

management: don’t leave scrap lying around to be eaten, etc.

75
Q

Afib in cattle typically caused by

A

acid-base & electolyte disturbances secondary to GIT dz

- hypocalcemia, hypokalemia, hypochloremia, metaboic alkalosis

76
Q

describe the sound of afib on ascultation

A

irregularly irregular rhythm

77
Q

ECG findings indicative of afib

A

irregular RR interval, no P waves, f wave, irregular QT intervals

78
Q

treatment for afib

A

**treat underlying cause - GIT dz, correct the electrolyte and acid-base abnormalities
can do quinidine conversion, in cattle
can do elecro conversion in small ruminants