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CPR II Exam 1 > Chapter 12/Lecture 7: Cardiac Specializations, Aging, CHF, Congenital/Ischemic Heart Dz > Flashcards

Chapter 12/Lecture 7: Cardiac Specializations, Aging, CHF, Congenital/Ischemic Heart Dz Flashcards

1
Q

In pt’s with what underlying disease may the onset of an MI be completely asymptomatic?

How is the disease discovered?

A
  • Diabetic neuropathy
  • Discovered ONLY by EKG and lab findings
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2
Q

What are the most sensitive and specific markers of myocardial damage?

A

cTnT and cTnI

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3
Q

Why is CK-MB a sensitive but not specific marker for myocardial damage?

A

Can also be elevated after skeletal m. injury

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4
Q

How many hours post-MI do levels of CK-MB, cTnT and cTnI begin to rise in the serum?

A

3-12 hours

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5
Q

After how many hours are levels of cTnI and CK-MB at their maximum levels following myocardial damage?

A

24 hours

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6
Q

How long after myocardial damage does it take for CK-MB, cTnI and cTnT levels to normalize?

A
  • CK-MB = 48-72 hours
  • cTnI = 5-10 days
  • cTnT = 5-14 days
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7
Q

Half of all MI deaths occur within 1 hour of onset, and are usually secondary to what complication?

A

Arrhythmia

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8
Q

What is the contractile dysfunction following an MI proportional to?

Severe “pump failure” can lead to what potentially lethal complication?

A
  • Size of the infarct
  • Cardiogenic shock = 70% mortality rate
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9
Q

Myocardial rupture following an MI occurs when there is what type of necrosis?

A

Transmural

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10
Q

What is the most common site of myocardial rupture seen following an MI and complications that ensue?

A
  • Rupture of the ventricular free wall (anterolateral wall at mid-ventricular levels)

- Hemopericardium and cardiac tamponade

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11
Q

Myocardial rupture occurring as a complication post-MI most often occurs when and is due to what?

A
  • 2-4 days after MI
  • When coagulative necrosis + neutrophilic infiltrate + lysis of myocardiac CT —> weaken infarcted myocardium
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12
Q

What is a late complication of large transmural myocardial infarcts that experience early expansion?

A

Ventricular aneurysm = True aneurysm

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13
Q

What are 3 possible complications of ventricular aneurysms occurring post-MI?

A
  • Mural thrombus
  • Arrhythmias
  • Heart failure = most common complication
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14
Q

Large transmural myocardium infarcts have a higher probability of which 3 potentially lethal complications?

A
  • Cardiogenic shock
  • Arrhythmias
  • Late CHF
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15
Q

Ventricular remodeling post-MI involves what 2 compnsatory changes occurring in the non-infarcted segments?

A

Hypertrophy and Dilation

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16
Q

Hearts from patients with chronic IHD (ischemic cardiomyopathy) have what gross morphological changes?

A

Cardiomegaly w/ LV hypertrophy and dilation

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17
Q

Which congenital heart disease presents as early cyanosis - “blue babies?”

A

Right-to-left shunts

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18
Q

What are the 5 T’s associated with right-to-left shunts?

A
  1. Truncus arteriosus (1 vessel)
  2. Transposition (2 switched vessels)
  3. Tricuspid atresia (Tri = 3)
  4. Tetraology of fallot (Tetra = 4)
  5. TAPVR (5 letters) = total anomalous pulmonary venous connection
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19
Q

What occurs in Eisenmenger Syndrome?

Consequences include?

A
  • Uncorrected left-to-right shunt (VSD, ASD, PDA) –> ↑ pulmonary blood flow –> remodeling of vasculature –> pulmonary arterial HTN
  • RVH occurs to compensate –> shunt becomes right to left (reversal)
  • Causes: late cyanosis, clubbing, and polycythemia
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20
Q

How does pressure-overload hypertrophy differ from that of volume-overload in terms of myocyte and ventricular changes?

A
  • P.O. = myocytes thicken w/ concentric increase in wall thickness
  • V.O. = myocytes elongate and ventricles dilate; wall thickness may be increased, normal, or decreased
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21
Q

A hypertrophied heart is vulnerable to?

A

Ischemia-related decompensation

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22
Q

Aerobic exercise tends to be associated with volume-overload hypertrophy that may be accompanied by what other compensatory mechanism not seen in pathological hypertophy?

A

Increase in capillary density

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23
Q

Clinical and morphological effects of left-sided CHF are a consequence of what?

A
  • Congestion of pulmonary circulation
  • Decreased perfusion of down-stream tissues –> organ dysfunction
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24
Q

Most common morphology of the LV in left-sided heart disease?

A

Hypertrophied and massively dilated

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25
Q

Kerley B and C lines noted on CXR are associated with CHF of which side?

A

Left-sided CHF

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26
Q

Which type of immune cells are seen in the lungs of pt with left-sided CHF and are a telltale sign of previous episodes of pulmonary edema?

A

Heart failure cells = Hemosiderin-laden macrophages

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27
Q

Cough, dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspneas are all signs of what type of CHF?

A

Left-sided CHF

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28
Q

A reduced ejection fraction in left-sided CHF leads to diminished renal perfusion and resultant activation of what?

Exacerbates what?

A
  • Activates RAAS —> Na+ and H2O retention
  • Exacerbates ongoing pulmonary edema
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29
Q

In left-sided CHF due to diastolic failure, the LV is stiff and cannot relax during diastole, so any increase in filling pressure is immediately transferred where and leads to?

A

Back into pulmonary circulation = rapid onset pulmonary edema (flash pulmonary edema)

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30
Q

Diastolic failure of left-sided CHF is seen more commonly in which sex and what is the most common underlying etiology?

A
  • Women >65 yo
  • HTN is most common etiology
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31
Q

The common feature of the disorders that cause primary right-sided CHF (aka cor pulmonale) is what?

A

Pulmonary HTN

*1’ pulmonary HTN, recurrent pulmonary thromboembolism, and conditions causing pulmonary vasocontriction (i.e., obstructive sleep apnea, and altitude sickness)

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32
Q

Where are the major effects seen in right-sided CHF vs. left-sided?

A
  • Mainly in the systemic and portal venous systems
  • Pulmonary congestion is minimal (unlike in left-sided)
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33
Q

Hepatosplenomegaly, nutmeg liver, centrilobular necrosis and cardiac cirrhosis are all seen in what type of CHF?

A

Right-sided CHF

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34
Q

Systemic venous congestion in right-sided CHF can lead to fluid accumulations in which spaces?

A
  • Pleural, pericardial, or peritoneal spaces
  • Effusions
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35
Q

Edema in which areas of the body are a hallmark of right-sided CHF?

A
  • Peripheral and dependent portions of body, especially ankle (pedal) and pretibial edema
  • Generalized massive edema (anasarca) may occur
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36
Q

Renal congestion w/ greater fluid retention and more pronounced azotemia is more pronounced in CHF of which side?

A

Right-sided CHF

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37
Q

What is the single most common genetic cause of congenital heart disease?

A

Trisomy 21 - Down syndrome

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38
Q

GATA4 + TBX5 + NKX2-5 are TF’s implicated in what types of congenital heart defects?

A

Atrial and ventricular septal defects

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39
Q

Pt’s with down syndrome have one or more heart defects, most often affecting structures derived from which heart field?

A

2nd heart field (i.e., AV septae) = endocardial cushions

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40
Q

Mutations in which gene are associated with bicuspid aortic valve?

A

NOTCH1

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41
Q

Mutations in which 2 genes are implicated in Tetralogy of Fallot?

A

JAG1 and NOTCH2

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42
Q

Deletion of chromosome 22q11.2 is associated with what syndrome?

A

DiGeorge syndrome

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43
Q

Which gene located on chromosome 22q11.2 is the most likely culprit of cardiac abnormalities seen in deletion of this chromosome?

Gene is reponsible for regulating what?

A

TBX1 –> regulates NCC migration

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44
Q

The deficits associated with DiGeorge syndrome can be remembered using CATCH-22, what are they?

A
  • Cardiac abnormality
  • Abnormal facies
  • Thymic aplasia
  • Cleft palate
  • Hypocalcemia
  • All on chromosome 22
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45
Q

Which chromosomal aneuploidies are most often associated with congential heart defects?

A

Turner syndrome (monosomy X) and trisomies 13, 18, 21

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46
Q

What are 3 enviornmental factors that alone or in combo w/ genetic factors are implicated in congenital heart disease?

A
  • Congenital rubella
  • Gestational diabetes
  • Teratogen exposure
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47
Q

Which type of left-to-right defect causes an increase in RV and pulmonry outflow volumes only?

48
Q

Which 2 left-to-right defects cause an increase pulmonary blood flow and pressure?

A

VSD and PDA

49
Q

Left-to-right shunting causes volume overload on the right side which may lead to what 2 complications?

A
  • Pulmonary HTN

- Reversal (L–>R becomes R–>L = Eisenmenger syndrome)

  • Right heart failure
50
Q

Paradoxical embolism is associated with what kind of shunt?

A

Right —> Left

*Emboli from veins bypass the lungs and directly enter systemic circulation

51
Q

Severe long-standing cyanosis associated with right-to-left shunts can cause what do conditions?

A
  • Clubbing of fingers and toes = hypertrophic ostroarthropathy
  • Polycythemia
52
Q

Which type of ASD is not associated w/ other anomalies, may be of any size, and can be multiple or fenestrated?

A

Secundum ASD

53
Q

Which location for an ASD is the most common?

A

Septum Secundum ASD

54
Q

Which type of murmur may be associated with an ASD?

A

Pulmonary valve murmur; Pulm. blood flow = 2-8x normal

55
Q

At what age do ASD’s generally become symptomatic?

A

Usually not before age 30

56
Q

In pt’s with a patent foramen ovale what events can cause the unsealed flap to open and produce brief periods of right-to-left shunting?

Possible complication?

A
  • Anything that can ↑ right-sided pressures
  • Pulmonary HTN + Bowel movement + Coughing + Sneezing
  • Complication = paradoxical emboli
57
Q

90% of VSD’s occur in which region and are classified as?

A

Membranous interventricular septum = Membranous VSD

58
Q

Functional consequences of VSD’s are dependent on what?

59
Q

Large VSDs can cause what 2 complications and almost universally lead to what overtime?

A
  • Early RV hypertrophy
  • Pulmonary HTN —(over time)–> IRREVERSIBLE PVD; shunt reversal, cyanosis, and death
60
Q

PDA can arise due to delayed closure in infants with?

A

- Hypoxia (due to respiratory distress or heart disease)

- Presence of VSD, which ↑ pulmonary vascular pressures

61
Q

A harsh “machinery-like” murmur is characteristic of what congenital heart defect?

62
Q

What are the 4 cardinal features of Tetraology of Fallot?

*Use the mnemonic PROVe

A

1) SubPulmonary stenosis (obstruction of the RV outflow tract)
2) RV hypertrophy
3) Overriding aorta
4) VSD

63
Q

What does the clinical severity of Tetralogy of Fallot depend on?

A

Degree of subpulmonary stenosis, since this determines direction of flow

64
Q

Classic TOF is associated with what degree of stenosis and has what consequences?

A

Severe stenosis –> right-to-left shunt -> cyanosis

65
Q

Mild stenosis in TOF resembles what and has what type of shunt?

A

Resembles VSD w/ L to R shunt

66
Q

Majority of infants with TOF are what at birth?

67
Q

Transpositon of the Great Arteries is not compatible with life unless what is present?

A

Shunt for adequate mixing of blood (VSD, PDA, or PFO)

68
Q

What occurs in the RV and LV in pt’s with Transposition of the Great Arteries?

A
  • RV hypertophy due to functioning as systemic ventricle
  • LV becomes thin-walled (atrophic)
69
Q

Coarctation of the Aorta is common in which sex and seen in which chromosomal disease?

A
  • 2x more common in males
  • Females w/ Turner syndrome are more commonly affected
70
Q

How does the infantile form differ from the adult form of Coarctation of the Aorta?

A
  • Infantile = tubular hypoplasia of aortic arch proximal to PDA
  • Adult = discrete ridge-like infolding of aorta distal to ligamentum arteriosum
71
Q

50% of cases of Coarctation of the Aorta are accompanied by what valvular anomaly?

A

Bicuspid aortic valve

*May also be assoc. w/ congenital aortic stenosis, ASD, VSD, mitral regurgitation, or berry aneursyms of the circle of Willis

72
Q

When does coarctation of the aorta WITH PDA usually manifest and what are the sx’s?

A
  • Manifests AT BIRTH
  • Cyanois localized to lower half of body
73
Q

How does coarctation of the aorta WITHOUT PDA typically manifest?

Characteristic signs and sx’s?

A
  • Usually asymptomatic at birth
  • Adults = HTN in the UE’s w/ HYPOtension + weak pulses in LE’s
  • Claudication and cold LE’s due to low blood flow
  • Development of collateral circulation thru enlarged intercostal internal mammary as. –> Rib notching (on radiographs)
74
Q

Which ausculatory finding may be appreciated with coarctation of the aorta?

Which ventricle undergoes adaptive change?

A
  • Murmur w/ vibratory “thrill”
  • Concentric LV hypertrophy
75
Q

Hypoplastic left heart syndrome due to obstruction of LV outflow due to severe congenital aortic stenosis or atresia leads to what 3 morphological findings?

A
  • LV HYPOplasia
  • HYPOplasia of the aorta
  • Porcelain-like LV endocardial fibroelastosis
76
Q

Thickened ring or collar of dense endocardial fibrous tissue below the level of the aortic valve cusps is characteristic of which variation of aortic stenosis?

A

Subaortic stenosis

77
Q

What must be maintained in severe congenital aortic stenosis or atresia to prevent death?

A

Preservation of PDA patency

78
Q

Which variation of aortic stenosis/atresia is associated with a prominent systolic murmur and sometimes a thrill?

A

Subaortic stenosis

79
Q

Supravalvular aortic stenosis is sometimes a component of which syndrome resulting from the deletions of which gene and on which chromosome?

A
  • Williams-Beuren Syndrome –> hypercalcemia, facial anomalies, cognitive abnormalities, and aortic stenosis
  • Elastin gene on chromosome 7
80
Q

What are the 2 most common congenital conditions responsible for right-to-left shunts?

A
  • TOF
  • Transposition of great arteries (TGA)
81
Q

Majority (90%) of cases of IHD are secondary to?

A

Obstructive Atherosclerosis

82
Q

What are the 3 major coronary epicardial arteries involved by obstructive atherosclerosis in IHD?

A
  • LAD
  • Circumflex branch of LCA = LCX
  • RCA
83
Q

A fixed lesion obstructing >___% of vascular cross-section area defines significant CAD and is generally the threshold for symptomatic ischemia?

84
Q

Acute plaque change that induces abrupt thrombotic occlusion, resulting in myocardial necrosis defines what?

A

Myocardial Infarction (MI)

85
Q

Paroxysmal and recurrent attacks of chest pain induced by myocardial ischemia insufficient to induce myocyte necrosis (MI) is characteristic of?

A

Angina Pectoris

86
Q

Severe angina or chest discomfort, described as frank pain that is increasing in frequency, duration, and severity precipitated by lower levels of physical activity or even at rest is characteristic of?

A

Unstable (or “crescendo”) angina

87
Q

Unstable (or “crescendo”) angina is caused by what?

A

Disruption of atherosclerotic plaque w/ partial thrombosis and possibly embolization or vasospasm (or both)

88
Q

50% of pt’s w/ unstable (“crescendo”) angina have evidence of what?

A

Myocardial necrosis; acute MI may be imminent

89
Q

How soon after onset of severe ischemia does myocardial contractility cease?

A

Within 1 minute

90
Q

Severe ischemia (blood flow <10% normal) for how long is associated with irreversible damage of cardiac myocytes?

A

20-40 minutes

91
Q

Due to the myocardial perfusion pattern, ischemia is most pronounced in which layer and irreversible injury occurs in which zone first?

A
  • SUBendothelial layer = most pronounced ischemia
  • SUBendothelial zone = 1st to undergo irreversible injury
92
Q

How many hours after onset of myocardial ischemia is half the thickness of the myocardium necrotic and how many hours for transmural necrosis?

A
  • 1/2 thickness = 2-3 hours
  • Transmural = 6 hours

*Necrosis moves from SUBendocardium –> epicardium

93
Q

The LAD supplies which 3 areas of the myocardium?

A
  • Apex
  • Anterior wall of LV
  • Anterior 2/3’s of septum
94
Q

The RCA supplies which 3 areas of the myocardium?

A
  • Entire RV free wall
  • LV posterior wall
  • Posterior 1/3 of septum
95
Q

The LCX generally only supplies which area of the myocardium?

A

Lateral wall of LV

96
Q

What is the myocardial damage like in subendocardial (nontransmural) infarction that occur as a result of global hypotension?

A

Damage usually circumferential, rather than being limited to distribution of single major coronary artery

97
Q

Subendocardial (nontransmural) infarcts can occur due to plaque disruption followed by a coronary thrombus which undergoes what?

A

Lysis (therapeutically or spontaneously)

98
Q

Multifocal microinfarction involves smaller intramural vessels and most often occurs due to what?

A
  • Vasculitis
  • Microembolization
  • Vascular spasm –> epinephrine or cocain
99
Q

Why is there a narrow rim of preserved subendocardial myocardium even in a transmural infarction?

A

Due to diffusion of O2 and nutrients from the ventricular lumen

100
Q

What is the predominant mechanism of cell death (apoptosis/necrosis) following an MI and become detectable how long after onset?

A

Ischemic coagulative necrosis –> 6-12 hrs

101
Q

Immersion of tissue slices into a solution of what following death from an acute MI allows for the visualization of necrotic areas?

A

Triphenyl-tetrazolium chloride

102
Q

Which sublethal change may be seen in the margins of infarcts and reflects intracellular accumulation of Na+ and H2O within the sarcoplasmic reticulum?

A

Myocyte vacuolization or myocytolysis

103
Q

When can pyknosis of nuclei; myocyte hypereosinophilia; marginal contraction band necrosis; and early neutrophilic infiltrate be visualized microscopically post-MI?

A

12-24 hours

104
Q

How long post-MI will you see coagulation necrosis w/ loss of nuclei and striation; with neutrophilic infiltration?

105
Q

What is the gross morphology of heart 1-3 days post-MI?

A

Mottling w/ yellow-tan infarct center

106
Q

What is the gross morphology of heart 3-7 days post-MI?

A

Hyperemic border; central yellow-tan softening

107
Q

How long post-MI will you see beginning disintegration of dead myofibers w/ dying neutrophils and early phagocytosis of dead cells by macrophages?

108
Q

How many days post-MI will there be well-developed phagocytosis of dead cells w/ granulation tissue at margins?

109
Q

How many days post-MI will there be WELL-established granulation tissue w/ NEW blood vessels and collagen deposition?

A

10-14 days

110
Q

What is seen microscopically and grossly 2-8 weeks post-MI?

A

- Micro = increased collagen deposition, w/ decreased cellularity

- Gross = gray-white scar

111
Q

>2 months following an MI what will be seen microscopically?

A

DENSE collagenous scar = Scarring is complete

112
Q

How long post-MI can early coagulation necrosis + edema; hemorrhage be visualized?

A

4-12 hours

113
Q

Earliest detectable feature of myocyte necrosis via EM is disruption of what?

A

Sarcolemmal disruption; mitochondrial amorphous densities

114
Q

A heart that is maximally yellow-tan and soft w/ depressed red-tan margins is seen how long post-MI?

115
Q

Characteristic morphological finding of irreversibly injured myocytes following reperfusion?

A

Contraction bands

116
Q

Myocardium that is subjected to chronic, sublethal ischemia may enter into a state of lowered metabolism and function called what?

A

Hibernation

CPR II Exam 1 (25 decks)

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