Cardiac Path Robbins Part 2 Flashcards Preview

Cardiovascular II > Cardiac Path Robbins Part 2 > Flashcards

Flashcards in Cardiac Path Robbins Part 2 Deck (64)
Loading flashcards...

Right-to-left shunts- also called? involves?

cyanotic congenital heart disease!!!
-Tetralogy of Fallot- most common!
-transposition of great a's
-others- truncus arteriosus, tricuspid atresia, total anomalous pulm venous cconnection


Tetralogy of Fallot- 4 cardinal features

-an aorta that overrides the VSD
-obstruction of right ventricular outflow tract (subpulm stenosis)
-right ventricular hypertrophy
*result from anterosuperior displacement of the infundibular septum


Tetralogy of Fallot- morphology

-"boot-shaped" heart (due to right ventricular hypertrophy)
-large VSD with the aortic valve at the superior border, overriding the defect
-obstruction of right ventricular outflow due to subpulmonic stenosis (sometimes accompanied by pulm valvular stenosis)
-right aortic arch in 25% of cases


Tetralogy of Fallot- clinical featurs

-can survive into adult life w/o treatment
-depends on subpulm stenosis!!
-if mild stenosis- represents an isolated VSD- left-to-right shunt without cyanosis!! ("pink tetraology")
-if severe right ventricular outflow obstruction- right-to-left shunt!!- cyanosis!!! (classic TOF)


Transposition of the Great Arteries

-produces ventriculoarterial discordance!!
-aorta arises from right ventricle; pulm a from left ventricle
-abnormal formation of truncual and aortopulmonary septa
-1/3 have a VSD!
-2/3 have patent foramen ovale or PDA!
-separation of the systemic and pulm circulations- incompatible with postnatal life!!
-need a shunt!
-right venticular hypertrophy occurs
-die within months w/o surgery


Triscuspid Atresia

-complete occlusion of tricuspid valve orifice
-due to unequal division of AV canal- so mitral valve is larger than normal and right ventricular underdevelopment


Obstructive lesions

-coarctation of aorta
-pulm stenosis and atresia
-aortic stenosis and atresia


Coarctation of the aorta- affects? 2 forms

-2x in males; females with Turner syndrome
-"infantile" form- symptomatic in infancy- proximal to the PDA (patent ductus arteriosus)
-"adult" form- infolding of the aorta just opp the closed ductus arteriosus


Coarctation of the aorta with a PDA

-manifests early in life
-delivery of unsaturated blood thru PDA- cyanosis- R to L shunt
-need surgery to occlude the PDA!!


coarctation of the aorta without a PDA

-most kids are asymptomatic
-HTN in extremities
-weak pulses and hypotension in LEs
-development of collateral circulation b/w pre and post-coarctation a's- "notching" on xray


pulmonary stenosis and atresia

-obstruction at the level of the pulm valve
-can be with TOF (tetralogy of fallot) or TGA (transposition of great a's) or isolated
-right ventricular hypertrophy
-if atresia- hypoplastic right ventricle and an ASD


aortic stenosis and atresia- 3 locations

-valvular, subvalvular, supravalvular
-isolated 80%
-valvular- hypoplastic, dysplastic, or abnormal in number cusps
-if severe- obstruction of left ventricular outflow tract- hypoplasia of left ventricle and asc aorta- ductus must be open to allow blood flow to aorta!! (hypoplastic left heart syndrome)


ischemic heart disease- represents?

syndromes resulting from myocardial ischemia:
-angina pectoris (chest pain)
-chronic IHD with heart failure
-Sudden cardiac death


leading cause of death in the US

IHD (ischemic heart disease)


dominant cause of IHD syndomes

-insufficient coronary perfusion relative to myocardial demand
-mostly due to chronic, progressive atherosclerotic narrowing of the epicardial coronary a's and superimposed plaque change, thrombosis, and vasospasm


chronic vascular occlusion

->75% obstructed- significant CAD- threshold for symptomatic ischemia precipitated by exercise (compensatory vasodilaton no lunger sufficient)
-90% obstructed- inadequate blood flow at rest
-collateral vessels develop over time


acute plaque change

-acute coronary syndromes- unstable angina, acute MI, sudden death
-initiated by the conversion of a stable atherosclerotic plaque to an unstable life-threatening atherothrombotic lesion thru rupture, erosion, ulceration, fissuring, or deep hemorrhage
-in most cases- plaque changes results in a thrombus!!


consequences of myocardial ischemia- due to?

-stable angina- stenosed coronary a's
-unstable angina- plaque disruption- leads to thrombosis and vasoconstriction
-MI- acute plaque change- thrombotic occlusion
-sudden cardiac death- fatal ventricular arrhythmia due to regional myocardial ischemia


angina pectoris

-often recurrent chest pain induced by transient myocardial ischemia (15 s to 15 min) insufficient to induce MI (myocyte necrosis)
-pain due to ischemia-induced release of adenosine, bradykinin- stim sympathetic and vagal afferent n's


angina pectoris- 3 clinical variatns

-stable angina
-prinzmetal variant angina
-unstable (crescendo) angina


stable angina

stenotic occlusion of coronary a
-produced by physical activity, stress
-squeezing/burning sensation
-relieved by rest or vasodilators


prinzmetal variant angina

-episodic coronary a spasm, relieved with vasodilators


unstable (crescendo) angina

-frank pain, inc in frequency, duration (>20 min) and severity, eventually at rest
-usually rupture of a plaque, with a partial thrombus
-50% may have evidence of myocardial necrosis


MI- causes

90% from atheromatous plaque!!
-embolus (from left atrium due to atrial fibrillation; left-sided mural thrombus, vegetations of infective endocarditiis, paradoxical emboli)
-vasospasm (drugs, coronary atherosclerosis)
-ischemia secondary to vasculitis, shock, hematologic abnormalities


MI- pathogenesis- coronary arterial occlusion

-coronary a atheromatous plaque- acute change- hemorrhage, erosion/ulceration, rupture/fissuring
-exposed subendo collagen and necrotic plaque contents- platelets adhere- act release their granule ontentes- form microthrombi
-vasospasm stim by mediators released from platelets
-tissue factor- act complement pathway
-thrombus can expand to occlude the vessel within minutes


MI- classic presentation

MI- classic presentation -prolonged chest pain! (>30 min)- crushing, stabbing, squeezing, tightness, radiating down left arm/left jaw
-up to 25% are asymptomatic


time of onset of key events in ischemic cardiac myocytes

-ATP depletion- seconds
-loss of contractility- <2 min
-ATP reduced (50%- 10 min; 10%- 40 min)
-irreversible cell injury- 20-40 min
-microvascular injury- >1 hr


ischemia- most prominent where?

(due to the perfusion pattern from epicardium to endocardium)
-when more extended ischemia- wavefront of cell deati hmoves thru the myocadrium


MI- early changes- biochemical findings

-ATP dec
-lactate inc


irreversible phase- starts when?

30 min
-progressive loss of viability occurs that is complete by 6-12 hrs