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Cardiovascular II > Cardiac Path Robbins Part 2 > Flashcards

Cardiac Path Robbins Part 2 Flashcards

1
Q

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

A

cyanotic congenital heart disease!!!

  • Tetralogy of Fallot- most common!
  • transposition of great a’s
  • others- truncus arteriosus, tricuspid atresia, total anomalous pulm venous cconnection
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2
Q

Tetralogy of Fallot- 4 cardinal features

A
  • 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
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3
Q

Tetralogy of Fallot- morphology

A
  • “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
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4
Q

Tetralogy of Fallot- clinical featurs

A
  • 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)
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5
Q

Transposition of the Great Arteries

A
  • 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
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6
Q

Triscuspid Atresia

A
  • complete occlusion of tricuspid valve orifice

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

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7
Q

Obstructive lesions

A
  • coarctation of aorta
  • pulm stenosis and atresia
  • aortic stenosis and atresia
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8
Q

Coarctation of the aorta- affects? 2 forms

A
  • 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
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9
Q

Coarctation of the aorta with a PDA

A
  • manifests early in life
  • delivery of unsaturated blood thru PDA- cyanosis- R to L shunt
  • need surgery to occlude the PDA!!
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10
Q

coarctation of the aorta without a PDA

A
  • 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
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11
Q

pulmonary stenosis and atresia

A
  • 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
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12
Q

aortic stenosis and atresia- 3 locations

A
  • 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)
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13
Q

ischemic heart disease- represents?

A

syndromes resulting from myocardial ischemia:

  • MI
  • angina pectoris (chest pain)
  • chronic IHD with heart failure
  • Sudden cardiac death
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14
Q

leading cause of death in the US

A

IHD (ischemic heart disease)

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15
Q

dominant cause of IHD syndomes

A
  • 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
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16
Q

chronic vascular occlusion

A
  • > 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
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17
Q

acute plaque change

A
  • 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!!
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18
Q

consequences of myocardial ischemia- due to?

A
  • 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
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19
Q

angina pectoris

A
  • 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
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20
Q

angina pectoris- 3 clinical variatns

A
  • stable angina
  • prinzmetal variant angina
  • unstable (crescendo) angina
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21
Q

stable angina

A

stenotic occlusion of coronary a

  • produced by physical activity, stress
  • squeezing/burning sensation
  • relieved by rest or vasodilators
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22
Q

prinzmetal variant angina

A

-episodic coronary a spasm, relieved with vasodilators

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23
Q

unstable (crescendo) angina

A
  • 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
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24
Q

MI- causes

A

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
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25
Q

MI- pathogenesis- coronary arterial occlusion

A
  • 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
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26
Q

MI- classic presentation

A

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
27
Q

time of onset of key events in ischemic cardiac myocytes

A
  • 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
28
Q

ischemia- most prominent where?

A

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

29
Q

MI- early changes- biochemical findings

A
  • ATP dec

- lactate inc

30
Q

irreversible phase- starts when?

A

30 min

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

31
Q

progression of myocardial necrosis after coronary a occlusion

A
  • 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
32
Q

dominant a

A

coronary a (RCA or LCX)- post third of septm

33
Q

right dominant circulation

A

(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!!
34
Q

LAD (left anterior desc)- areas of infarct

A

(40-50%)

  • apex
  • LV anterior wall
  • ant 2/3 of septum
35
Q

RCA- areas of infarct

A

(30-40%)

  • RV free wall
  • LV posterior wall
  • post third of septum
36
Q

LCX (left circumflex)- areas of infarct

A

(15-20%)

-LV lateral wall

37
Q

patterns of infarction

A
  • transmural
  • subendocardial (nontransmural)
  • multifocal microinfarction
38
Q

transmural infarction

A
  • occlusion of epicardial vessel
  • necrosis involves the full thickness of the ventricular wall
  • usually assoc with chronic coronary atherosclerosis, acute plaque change, superimposed thrombosis
39
Q

subendocardial (nontransmural) infarction

A
  • 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)
40
Q

multifocal microinfarction

A
  • smaller intramural vessels
  • microembolization, vasculitis, vascular spasm (cocaine, epinephrine)
  • takotsubu cardiomyopathy (broken heart syndrome)
41
Q

STEMI and NSTEMIs

A
  • STEMI- transmural infarct

- NSTEMI- subendocardial infarct

42
Q

Triphenyltetrazolium chloride- stains what

A

-tissue containing lactate dehydrogenase- stained red

43
Q

morphologic evolution of MI- 1/2 hr- 24 hrs

A
  • 1/2-4 hrs- none

- 4-24 hrs- dark mottling; coagulation necrosis

44
Q

morphologic evolution of MI- 1- 10 days

A
  • 1-3 days- mottling, yellow-tan center; coag necrosis, many PMNs
  • 7-10 days- yellow-tan soft, phagocytosis of dead cells; granulation tissue
45
Q

morphologic evolution of MI- over time- > 10 days

A
  • 10-14 days- red-grey; granulation tissue, new vessels, collagen
  • 2-8 wks- grey-white scar; inc collagen
  • > 2 months- complete scar; dense collagen
46
Q

gross and microscopic appearance of an infarct depends on?

A

duration of survival of the pt following the MI

47
Q

reperfusion

A
  • 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”
48
Q

irreversibly injured myocytes- exhibit?

A

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!!!
49
Q

MI diagnosed by?

A
  • clinical symptoms
  • lab tests for myocardial proteins in plasma
  • electrocardiographic changes
50
Q

lab findings of MI

A

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
51
Q

CK-MB, cTnI, cTnT- return to normal- time?

A
  • CK-MB returns to normal in 48-72 hrs
  • cTnI 5-10 days
  • cTnT 5-14 days
52
Q

complications of MI

A

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
53
Q

other complications of MI

A
  • contractile dysfxn
  • fibrinous pericarditis
  • myocardial rupture
  • infarct expansion
  • ventrticular aneurysm
54
Q

myocardial rupture- occurs when? risk factors?

A
  • 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
55
Q

myocardial rupture- types

A
  • rupture of ventricular wall- most common!!
  • ventricular septum- acute VSD- left-to-right shunting
  • paipllary m rupture (least common)- mitral regurgitation
56
Q

infarct expansion

A
  • m necrosis- weakening, stretching and thinning of wall

- mural thrombus often seen

57
Q

ventricular aneurysm

A
  • late complication of large transmural infarcts with early expansion
  • composed of thinned wall of scarred myocardium
  • assoc with mural thrombus
  • rupture usually doesnt occur
58
Q

most common cause of rhythm disorders

A

ischemic injury!

  • Sa node- sick sinus syndrome
  • atrial fibrillation (irritable myocytes)
  • heart block (AV node dysfxnal)
59
Q

sudden cardiac death- causes

A
  • 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
60
Q

mechanism of SCD

A

-due to a fatal arrhythmia from ischemia-induced myocardial irritability

61
Q

left-sided hypertensive disease

A
  • 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
62
Q

diagnosis of systemic (left-sided) HTN disease

A
  • left ventricular hypertrophy

- HTN in other organs

63
Q

Pulmonary (right-sided) hypertensive disease (Cor Pulmonale)

A
  • due to pulm HTN

- acute cor pulmonale may arise from a large pulm embolus

64
Q

most common cause of pulm HTN

A

left-sided heart disease

Cardiovascular II (13 decks)

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