Cardio. Contusions. Chap 44 Flashcards

1
Q

most common consequence of myocardial contusion:

onset:

Dx:

R/O:

A

arrhythmias

may be delayed in onset up to 48 hours

Holter/ECG plus troponin (Direct visualization of the heart
or histologic examination current diagnostic gold standard)

normal ECG findings and cardiac troponin I levels on admission efficient R/O human trauma patients a normal cTnI level in combination with a normal ECG tracing on arrival has a negative predictive value of 100% for myocardial injuries

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2
Q

Tx:

Antiarrhythmics:

A

aimed toward maintaining optimal cardiac output and suppressing life-threatening arrhythmias

Antiarrhythmic therapy is not recommended if arterial pulse quality is good and synchronous on auscultation, MAP, not clinical

class I antiarrhythmic agents, including lidocaine and
procainamide
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3
Q

controversial

A

lack of consistent evidence that this injury has any effect on patient outcome

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4
Q

Blunt thoracic trauma has been reported to result in myocardial injuries ____

A

8% to 95% of human - similar in vet med

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5
Q

MoA:

Proarrhythmic mechanism:

A

concussive and shearing injury (compressive and concussive inj.)

-lowering of the ratio of effective refractory period to
action potential duration
-increase in the resting membrane potential (less negative) in damaged myocardial cells

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6
Q

The echocardiographic features of myocardial injuries

A

(1) increased end-diastolic wall thickness
(2) impaired contractility, indicated by wall motion
abnormalities and decreased fractional shortening
(3) increased echogenicity
(4) localized areas of echolucency consistent with
intramural hematomas

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7
Q

troponin
level increase within ___:
decrease within ___:

A

cardiac troponins T and I - cTnT and cTnI
4 to 6 hours
up to 7 days

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8
Q

MYOCARDITIS:
Myocarditis is:

Infectious agents (viral, bacterial, protozoal) may cause
myocardial damage via: 

Myocarditis can also be associated with (4 plus infectious):

A

inflammatory process involving the heart -myocytes, interstitium, or vascular tree

myocardial invasion, production of toxins, or activation of immune-mediated disease

physical agents (doxorubicin)
underlying metabolic disorders (uremia)
toxins (heavy metals)
physical agents (heat stroke)

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9
Q

Viral myocarditis:
Parvovirus:

why no more myocarditis -

A

1970s and early 1980s, when the parvovirus pandemic
first was recognized, puppies did not receive maternal antibodies:
-very = CHF and death
-older puppies (2 to 4 months) often died subacutely from CHF vs. dilated cardiomyopathy (DCM) as young adults

now all puppies are protected y maternal Ab (unless didn’t suckle)

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10
Q
Chagas’ disease:
caused by:
location:
transmission: 
infective stage: 
amastigotes do what in cells:
Dogs with clinical Chagas’ disease have:
A

Trypanosoma cruzi, a protozoal parasite
Chagas’ disease is the leading cause of DCM in humans of Latin America

Texas and Louisiana

insect vector (Reduviidae), and reservoir hosts include rodents, raccoons, opossums, dogs, cats, and humans

trypomastigote is the infective stage
but on entering host enters the reproductive stage and becomes an amastigote

multiply until the host cell ruptures

acute or a chronic syndrome
acute stage, circulating trypomastigotes may be
seen in a thick blood smear, and most dogs are brought for treatment sudden development of signs of right-sided heart failure (ascites, tachycardia, lethargy)

chronic Chagas’ disease may enter a quiescent stage free of clinical signs for months or even
years. Nervous system damage often causes ataxia and weakness in these patients

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11
Q

bacterial myocarditis:

parasitic in cats:

toxic:

A

staph., strep., Rickettsia rickettsii, Ehrlichia canis, and
Bartonella species

Toxoplasma gondii

doxorubricin

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12
Q

myocarditis dx.

A

difficult - Elevated cardiac troponin I plus history +/- titres i.e. T. cruzi for Chagas

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