Cardio. Contusions. Chap 44 Flashcards
most common consequence of myocardial contusion:
onset:
Dx:
R/O:
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
Tx:
Antiarrhythmics:
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
controversial
lack of consistent evidence that this injury has any effect on patient outcome
Blunt thoracic trauma has been reported to result in myocardial injuries ____
8% to 95% of human - similar in vet med
MoA:
Proarrhythmic mechanism:
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
The echocardiographic features of myocardial injuries
(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
troponin
level increase within ___:
decrease within ___:
cardiac troponins T and I - cTnT and cTnI
4 to 6 hours
up to 7 days
MYOCARDITIS:
Myocarditis is:
Infectious agents (viral, bacterial, protozoal) may cause myocardial damage via:
Myocarditis can also be associated with (4 plus infectious):
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)
Viral myocarditis:
Parvovirus:
why no more myocarditis -
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)
Chagas’ disease: caused by: location: transmission: infective stage: amastigotes do what in cells: Dogs with clinical Chagas’ disease have:
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
bacterial myocarditis:
parasitic in cats:
toxic:
staph., strep., Rickettsia rickettsii, Ehrlichia canis, and
Bartonella species
Toxoplasma gondii
doxorubricin
myocarditis dx.
difficult - Elevated cardiac troponin I plus history +/- titres i.e. T. cruzi for Chagas