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Hannah CPR > Heart Valves, failure, congenital ischemic DZ > Flashcards

Heart Valves, failure, congenital ischemic DZ Flashcards

1
Q

number one worldwide cause of mortality, and 1/3 cause of deaths in the US

A

heart disease (cardiovascular dz)

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2
Q

when would a patent PDA be induced and how

A

by PGE given to infant

-lifesaving in infants with obstruction of pulmonary or systemic outflow

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3
Q

increased pressure overload vs increased volume overload effects on myocytes seen in hypertrophy

A

pressure- causes concentric LV thickness increasing due to myocyte thickening

volume-ventricular dilation due to myocyte elongation (use heart wt vs wall thickness to measure severity)

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4
Q

what results from insufficient perfusion meeting the metabolic demands of the myocardium

A

ischemic heart dz

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5
Q

define reperfusion injury

A
  • superimposed injury following reperfusion of blood to area of infarct (“vulnerable myocardium” )
  • can cause hemorrhage and endothelial swelling that can further occlude the capillaries
  • mediated by stress, calcium overload, recruited inflammatory cells that produce free radicals
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6
Q

classic presentation of myocardial infarct

A 
>30 min chest pain 
crushing, stabbing, tightness in chest
radiation of pain down left arm or left jaw
sweating 
dyspnea 
N/V
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7
Q

define tetralogy of fallot

A
  1. pulmonary stenosis/obstruction (determines severity)
  2. VSD
  3. overriding Aorta
  4. RV hypertrophy (causing boot-shaped heart)
    a right to left shunt causing decreased O2 rich blood perfusion bc O2 rich and O2 poor blood mixed in heart
    -infantile cyanosis
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8
Q

PDA is ___type of shunt and forms due to ?

A

left-to-right shunt

  • PDA is when blood flows from aorta to pulmonary A. which occurs because of abnormal closure of ductus arteriosus to ligamentem arterosis bc of hypoxic infant or increased pulmonary vascular pressure seen in a VSD
  • in utero the ductus arteriosus is a small vessel between aorta and pulmonary A. intended for blood to be shunted from right to left to bypass lungs/pulmonary circulation
  • **hear machinery like murmur
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9
Q

define transposition of great arteries (TGA)

A

when the RV is connected to aorta and LV connected to pulmonary A.
-leads to a right to left shunt; RV hypertrophy (to support systemic circulation) and LV atrophy

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10
Q

most common type of VSD, and complications associated

A

membranous VSD in membranous intraventrcular septum ( vs infundibular VSD in muscular septum)

  • > 50% small VSD spontaneously close
  • large VSD can lead to left-to right shutnting with complications of RV hypertrophy, pulm HTN, possible cyanosis and death
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11
Q

most common congenital cause of congenital heart dz

A

trisomy 21

-usually second heart field derives (AV septum from defects of endocardial cushions (osmium primum, ASD, VSD)

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12
Q

when does blood flow to the myocardium via the coronary arteries take place

A

ventricular diastole (closure of aortic valve)

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13
Q

what are complications associated MIs

A
  1. arrhythmias (fatal or long-term)
  2. contractile dysfunction –> pump failure
  3. fibrinous pericarditis (“aka bread and butter” due to myocardial inflammation
  4. myocardial rupture (due to transmural infarct 2-4 days after MI; fatal usually)
  5. infarct expansion (muscle necrosis leads to weakened walls; mural thrombi seen)
  6. ventricular aneurysm ( late complication of transmural infarct, seen with mural thrombi and arrhythmias with possible heart failure, rupture uncommon)
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14
Q

what are the three types of angina pectoris

A
  1. stable angina (stenotic occlusion of coronary A. leading to burning sensation in chest that can be relieved by rest or vasodilators; induced by PA or stress
  2. Prinzmental variant angina (spasmodic; coronary artery spasms causing pain, can be relieved with vasodilators but unrelated to PA or stress)
  3. unstable- aka crescendo angina (pain increasing in frequency, duration, and severity at progressively lower levels of PA until eventually at rest. usually leads to rupture of plaque with partial thrombus; 50% show myocardial necrosis and an acute MI can be eminent)
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15
Q

what proteins are released by myocytes during an MI that can be used to in lab to evaluate the heart attack

A
  1. troponin T and I (best marker bc elevates 3-12 hours after and remain elevated longer than other proteins (1-2 weeks) and not normally in circulation at any other time)
    * sensitive and specific”
  2. CK-MB (creatine kinase in heart; sensitive but not specific to MI; rises 3-12 hours after MI, peaks at 24hr, declines 2-3days after) )
    * sensitive only*
  3. myoglobin can show MI but rapid decline makes it unuseful
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16
Q

mild subpulmunary stenosis vs large stenosis in TOF

A 
mild= left to right shunt
large= right to left shunting with cyanosis
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17
Q

what produces a harsh machine like murmur

A

PDA

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18
Q

what is the number 1 COD caused by an MI

A

a fatal arrhythmia occurs within 1 hour after MI onset

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19
Q

left sided heart failure vs right sided heart failure

A

left

  • most commonly bc myocardial ischemia, but also bc HTN, left-sided valve DZ, or primary myocardial DZ
  • causes pulmonary congestion -> edema with; decreased tissue perfusion and cyanosis; decreased GFR and renin release to increase volume with prerenal azotemia
  • LV hypertrophy/dysfunction seen with left atrial dilation
  • sx: cough, lung crackles, wheezing, tachypnea, exertion dyspnea, cyanosis, A-fib, paroxysmal nocturnal dyspnea
  • **HEART FAILURE CELLS SEEN (hemosideren-MO)

right

  • most commonly bc left-sided HF, but could be bc isolated pulmonary HTN
  • signs: marked venous dilation –> hepatic congestion–> nutmeg liver, hepatosplenomegaly, pleural/pericadial/peritoneal effusions, LE edema, renal congestion
  • sx: increased venous pressure, ascites, edema, hepatosplenolgy, weight gain, distended jugular veins, fatigue
20
Q

what causes circumferential subendocardial infarct

A

global hypotension involving reduced blood flow to LAD, RCA, and LCX

21
Q

what is the dx when the heart is unable to pump blood at a rate to meet peripheral demand (or can only do so with increased filling pressure) therefore inadequately perfusing the body

A

congestive heart failure [loss of myocardial contractility (systolic fxn) or loss of ability to fill the ventricle (diastolic fxn) ]
*common end stage of heart failure seen from ischemic heart dz or hypertension induced work overload

22
Q

normal signs of aging in a heart

A
  • inceased epicardial fat
  • myocardial basophilic degeneration (gray-blue byproducts of glycogen metabolism in cardiac myocytes)
  • reduced LV cavity size
  • lipfuscin granules in myocardium
  • valve calcification
  • valve fibrous thickening
  • mitral leaflets buckle toward left atrium –> MVP–> in creased in left atrial size
  • lambl excrescences (processes on closure lines of aortic and mitral valves)
  • aortic stiffening
  • fewer myocytes in myocardium
23
Q

leading COD in the US

A

ischemic heart dz (90% deriving from atherosclerosis)

24
Q

what part of the heart is supplied by the LAD, RCA, and LCX

A

LAD - apex, LV anterior wall, anterior 2/3 of septum
RCA- RV free wall, LV posterior wall, and posterior 1/3 of septum
LCX- LV later wall
**in 80% of people with right dominant circulation

25
Q

what complications of MIs are associated with mural thrombi

A

infarct expansion and ventricular aneurysm

26
Q

3 types of damage that can occur to heart valves

A
  1. damage to collagen that weakens the leaflets (seen in MVP )
  2. nodular calcification beginning in the interstitial cells (found in all 3 layers) (ex: calcific aortic stenosis)
  3. fibrotic thickening (ex. seen in rheumatic heart dz)
    * thicken, weaken, or calcify
27
Q

where is atrial naturietic peptide stored

A

atrial myocytes in myocardium of heart

-causes vasodilation and renal salt and water elimination

28
Q

what is a PFO and how does it form

A
  • hole in atrial wall due to foramen ovale disclosure
  • in utero the foramen ovale with overlying flap that act as a valve only allowing blood to flow from right atrium to left , allows O2 rich blood from the umbilical vein and IVC to bypass pulmonary circulation
29
Q

an abnormal communication between chamber or blood vessels causing blood to flow down its gradient (high –> low) in abnormal locations

A

shunts

*left–> right is most common

30
Q

how to achieve reperfusion following an MI

A

thrombolysis (dissolve at risk blood clots in vessels and increase blood flow)
angioplasty
stent placement
CABG

31
Q

hypertrophied hearts are at increased risk of ____ due to no increase in blood supply to thickened myocardium

A

ischemic heart dz and heart failure

-can also lead to arrtyhmias

32
Q

when do eosinophils, neutrophils, MO, granulation tissue and collagen scar appear following an MI

A 
esoinophils - 12-24hr  (1/2 day) 
neutrophils -1 day 
MO-1 week 
granulation tissue - 10 days
scar - after 2 months (increased collagen begins at 2 weeks)
33
Q

Troponin I vs T in MI evaluation

A

both rise 3-12 hours following MI
cTnT peaks at 12-48 hours; return NL 5-14 days later
cTnI peak at 24 hours; return NL 5-10 days later

34
Q

will a Right to left or left to right shunt cause cyanosis early in life

A

right to left aka “cyanotic congenital heart dz”

35
Q

ASD vs VSD vs PDA effects on pulmonary circulatory volumes and pressure

A

ASD only increases outflow volume; VSD and PDA increase pulm blood flow and pressure

36
Q

TGA with VSD vs without VSD

A
  • 1/3 have VSD; have stable shunt
  • 2/3 have no VSD but have patent foramen ovale or PDA or surgically induced one in order to promote right to left shunting and adequate perfusion
37
Q

define coarctation of the aorta and its two types

A
  • narowing of the aorta
    1. “infantile form” -aortic arch tubular hypoplasia proximal to PDA leads to decreased left pressure near PDA and a right to left shunt. this causes cyanosis in lower half of body and requires early intervention for survival
    2. “adult form” - infolding of aorta opposite the closed PDA. can go unrecognized until adult life. expressivity depends on severity. usually see HTN in UE and weak pulses in LE with cold LE, and concentric LV hypertrophy. commonly seen in collateral circulation formation around the coarctation with intercostal and internal mammary A. showing “notching” of ribs on X-ray
38
Q

NOTCH 1 and NOTCH2/JAG1 relation to congenital heart dz

A

Notch1 - bicuspid aortic valve

Notch2/jag - tet of fallot (alagile syndrome)

39
Q

common population seen with aortic coarctation

A

2x more in males vs females and common in Tuners patients (XO)

40
Q

ASD is a ___ type of shunt and forms due to? list side effects of ASD

A

left-to-right shunt

  • usually failure of septum secundum to form at center of atrial wall (less commonly septum prism anomaly or sinus venous defects)
  • complications of volume overload on right side: right sided heart failure, paradoxical embolization, pulmonary vascular DZ , hear a murmur
41
Q

define angina pectoris

A

-is a transient often recurring chest pain induced by myocardial ischemia insufficient to induce a full infarct (MI)

42
Q

causes of cardiac hypertrophy

A

sustained pressure (HTN) or volume overload (aortic stenosis) or sustained trophic signaling (B1 stimulation)

43
Q

what indicates irreversible injury in an MI that normally occurs 20-40 minutes following an infarct

A

lactate levels increase (seen after 20 min)

also ATP levels begin to decrease in seconds

44
Q

T/F
severe pump failure, aka “cardiogenic shock” can be see after large MIs with >40% of LV and have 70% mortality and being the cause of 2/3 of in-hospital deaths related to admitted MI patients)

A

true

45
Q

define fibrosa, spongiosa, and ventricularis/artialis of valves

A

the middle layers between heart valve endothelium that are connected to valvular supporting structures

layer 1. -fibrosa- dense collagenous core on outflow surfaces (mechanical integrity fxn)

spongiosa- central core of loose connective tissue in middle (facilitates interaction between two layers)

ventricularis/atrialis - layer rick in elastin on the inflow surface (rapid recoil for valve closure fxn)

46
Q

define eisenmenger syndrome

A

rare
a complication arising when a severe Left to right shunt becomes a right to left shunt causing cyanosis
-due to irreversible damage to wall of pulmonary A. causes increasingly high right sided pressure forcing O2 poor blood from right to left
-also cause RV hypertrophy

47
Q

define prerenal azotemia

A
  • most common cause of acute renal failure

- lack of blood flow to kidneys resulting in excess nitrogen in blood

Hannah CPR (7 decks)

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