Cardiac Path Robbins Part 2 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
- VSD
- 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:
- MI
- 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
- diaphoresis!
- dyspnea
- nausea-vomiting
- 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?
-subendocardium
(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
progression of myocardial necrosis after coronary a occlusion
- begins beneath endocardial surface
- area that depends on the occluded vessel for perfusion- “at risk”
- a small narrow zone of myocardium beneath the endocardium is spared from necrosis b/c it can be oxygenated by diffusion from the ventricle
dominant a
coronary a (RCA or LCX)- post third of septm
right dominant circulation
(80% of individuals)
- RCA supplies the entire ventricular free wall, posterobsal wall of left ventricle, post 1/3 of ventricular septum
- LCX- lateral wall of left ventricle
- so RCA occlusions- left ventricular damage!!
LAD (left anterior desc)- areas of infarct
(40-50%)
- apex
- LV anterior wall
- ant 2/3 of septum
RCA- areas of infarct
(30-40%)
- RV free wall
- LV posterior wall
- post third of septum
LCX (left circumflex)- areas of infarct
(15-20%)
-LV lateral wall
patterns of infarction
- transmural
- subendocardial (nontransmural)
- multifocal microinfarction
transmural infarction
- occlusion of epicardial vessel
- necrosis involves the full thickness of the ventricular wall
- usually assoc with chronic coronary atherosclerosis, acute plaque change, superimposed thrombosis
subendocardial (nontransmural) infarction
- most vulnerable to any reduction in coronary flow (least perfused region of myocardium)
- inner third of ventricular wall- result of plaque disruption- coronary thrombus that becomes lysed before necrosis extends across the whole wall!!
- prolonged reduction in systemic BP (shock)
multifocal microinfarction
- smaller intramural vessels
- microembolization, vasculitis, vascular spasm (cocaine, epinephrine)
- takotsubu cardiomyopathy (broken heart syndrome)
STEMI and NSTEMIs
- STEMI- transmural infarct
- NSTEMI- subendocardial infarct
Triphenyltetrazolium chloride- stains what
-tissue containing lactate dehydrogenase- stained red
morphologic evolution of MI- 1/2 hr- 24 hrs
- 1/2-4 hrs- none
- 4-24 hrs- dark mottling; coagulation necrosis
morphologic evolution of MI- 1- 10 days
- 1-3 days- mottling, yellow-tan center; coag necrosis, many PMNs
- 7-10 days- yellow-tan soft, phagocytosis of dead cells; granulation tissue
morphologic evolution of MI- over time- > 10 days
- 10-14 days- red-grey; granulation tissue, new vessels, collagen
- 2-8 wks- grey-white scar; inc collagen
- > 2 months- complete scar; dense collagen
gross and microscopic appearance of an infarct depends on?
duration of survival of the pt following the MI
reperfusion
- restoring blood flow to an area of ischemia
- attempt to limit the infarct size by rescuing at risk myocardium
- thrombolysis, angioplasty, stent placement, CABG
- “time is myocardium”
irreversibly injured myocytes- exhibit?
contraction bands (eosinophilic intracellular stripes of closely packed sarcomeres)
- result from exaggerated contraction of sarcomeres when perfusion is reestablished (damaged membranes- high conc of Ca from plasma)
- reperfusion alters the morphology of lethally injured cells!!!
MI diagnosed by?
- clinical symptoms
- lab tests for myocardial proteins in plasma
- electrocardiographic changes
lab findings of MI
proteins escaping irreversibly damaged myocytes!
- troponin I and T (cTnI/cTnT)- most cardiac myocyte specific!!
- time to elevation of CKMB, CtnT and CtnI- 3-12 hrs
- CK-MB and cTnI peak- 24 hrs
CK-MB, cTnI, cTnT- return to normal- time?
- CK-MB returns to normal in 48-72 hrs
- cTnI 5-10 days
- cTnT 5-14 days
complications of MI
arrhythmia!
- 1/2 of all MI deaths occur within 1 hr of onset, are secondary to an arrhythmia
- can be a longer-term complication of MI- due to permanent damage to the conducting system, or from myocardial “irritability” following the infarct
other complications of MI
- contractile dysfxn
- fibrinous pericarditis
- myocardial rupture
- infarct expansion
- ventrticular aneurysm
myocardial rupture- occurs when? risk factors?
- typically requires a transmural infarct
- 2-4 days post MI- when infl and necrosis have weakened the wall
- risk factors- inc age, large transmural anterior MI, first MI, absence of LV hypertrophy
- ventricular rupture less common with prior MI- scarring inhibits myocardial tearing
myocardial rupture- types
- rupture of ventricular wall- most common!!
- ventricular septum- acute VSD- left-to-right shunting
- paipllary m rupture (least common)- mitral regurgitation
infarct expansion
- m necrosis- weakening, stretching and thinning of wall
- mural thrombus often seen
ventricular aneurysm
- late complication of large transmural infarcts with early expansion
- composed of thinned wall of scarred myocardium
- assoc with mural thrombus
- rupture usually doesnt occur
most common cause of rhythm disorders
ischemic injury!
- Sa node- sick sinus syndrome
- atrial fibrillation (irritable myocytes)
- heart block (AV node dysfxnal)
sudden cardiac death- causes
- w/o symptoms or within 1-24 hrs of symptom onset
- Coronary a disease- precipitates SCD in 80-90%
- other causes- cardiomyopathies, myocarditis, congenital abnormalities of conduction system, myocardial hypertrophy
mechanism of SCD
-due to a fatal arrhythmia from ischemia-induced myocardial irritability
left-sided hypertensive disease
- pressure overload results in left ventricular hypertrophy- LV wall is concentrically thickened
- diastolic dysfxn can result in left atrial enlargement- can lead to atrial fibrillation
- may lead to CHF
- risk factor for SCD
diagnosis of systemic (left-sided) HTN disease
- left ventricular hypertrophy
- HTN in other organs
Pulmonary (right-sided) hypertensive disease (Cor Pulmonale)
- due to pulm HTN
- acute cor pulmonale may arise from a large pulm embolus
most common cause of pulm HTN
left-sided heart disease
