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CPR II Exam 1 > Lecture 2: Cardiac Pathology Part 1 (Hillard) > Flashcards

Lecture 2: Cardiac Pathology Part 1 (Hillard) Flashcards

1
Q

How is Right vs Left dominance of the heart determined?

A
  • whichever side the posterior descending artery originates from is the dominant side

Right Dominant: supplied by Right Coronary Artery (RCA in 70%)

Left Dominant: supplied by Left Circumflex Artery (LCX in 10%)

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2
Q

What are some common changes seen in the aging heart? (EF/LA/BD/ML/SA)

A
  • inc. epicardial fat, lipofuscin accumulation (tan-brown), basophilic degeneration, myocyte loss

amyloid deposit of transthyretin –> senile amyloidosis (HEART FAILURE)

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3
Q

Cardiovascular Dysfunction

What are common reasons for Pump Failure, Flow Obstruction, and Regurgitant Flow?

A

PF: inadequate contraction (systole) or filling (diastole)

FO: inc. resistance (valve stenosis/HTN) or dec. blood flow (atherosclerosis –> cardiac ischemia)

RF: incompetent valves (vascular disease)

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4
Q

Cardiovascular Dysfunction

What are common reasons for Shunted Flow, Conduction Abnormalities, and Vessel Rupture?

How do motor vehicle collisions damage the aorta?

A

SF: congenital disease (VSD/PDA), after myocardial infarct –> ventricular septal rupture

CA: ischemic injury (infarct/nodal injury/dilated) or heritable arrhythmias

VR: aortic dissection or trauma (motor vehicle trauma)

  • ligamentum arteriosum gets torn from aorta
  • causes rapid, life-threatening hemorrhage
  • 2nd most common cause of death in MVC
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5
Q

What is the best measure of heart hypertrophy?

A

WEIGHT

  • hypertrophy = inc. muscle mass of thickened heart due to inc. cardiomyocyte size/length
  • cardiomegaly = abnormal enlargement, which can have an increased weight/size; dilated hearts will appear larger but will not weight more simply because they are expanded
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6
Q

How do myocytes of the heart change when exposed to pressure overload vs volume overload?

A

Pressure Overload:

  • concentric hypertrophy of ventricle
  • sarcomeres added in parallel (thicken)

Volume Overload:

  • dilation of ventricles
  • sarcomeres added in series (lengthen)
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7
Q

What is Congestive Heart Failure and what are two common causes of disease?

A
  • common, progressive condition caused by pump failure –> inadequate blood delivery (common end stage of many heart diseases)
  • loss of ability to FILL the VENTRICLES during diastole (ventricle too stiff/thick) OR loss of myocardial CONTRACTILE function during systole (dilated/enlarged heart)
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8
Q

What are common causes of Systolic (3) and Diastolic (3) Dysfunction?

A

S: ischemic injury, dilated cardiomyopathy, valve regurg.
- DECREASED ejection fraction

D: HTN, aortic stenosis, hypertrophic/restrictive cardiomyopathy

  • NORMAL ejection fraction, lower total volume
  • also caused by fibrosis (radiation/amyloid)
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9
Q

What are 3 main causes of Left-sided Heart Failure and what does it cause clinically (Forward vs Backward Failure)?

A

causes: myocardial ischemia, HTN, left-sided valve disease

clinical:
- pulmonary congestion/edema (cough, crackles, wheezes = “backwards failure”)
- dec. tissue perfusion (cerebral, renal = azotemia: inc. creatinine and blood/urea nitrogen lvls = “forward failure”)

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10
Q

What is seen on chest x-ray of pts. with Left Heart Failure and what is a histological hallmark of heart failure?

A

X-Ray –> Kerley B lines

  • not specific
  • short, parallel lines that reach lung periphery

Histo: hemosiderin-laden macrophages

  • “Heart Failure Cells”
  • see brown macrophages in alveolar space of lungs
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11
Q

What is the most common cause of Right Heart Failure?

A

Left Heart Failure

  • causes inc. pulmonary pressure
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12
Q

What is Cor Pulmonale and what is it commonly caused by?

How do pts. present clinically? (4 major)

A

CP = isolated right-sided failure (pulmonary HTN)

  • parenchymal lung disease (MOST COMMON)
  • also lung thromboemboli, primary pulm. HTN (rare)

clinical: hepatosplenomegaly (congestion), distended jugular veins, effusions (peritoneal, pleural, pericardial), edema (gravity dependent), weight gain (fluid accum.)

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13
Q

What does the liver of a pt. with Congestive Heart Failure look like on biopsy?

What emboli can cause Saddle Embolism/Pulmonary Thrombus formation?

A
  • centriolobular hemorrhage and necrosis due to central vein congestion
  • “Nutmeg Liver” due to passive congestion

Saddle Embolism/Pulmonary Thrombus:
- DVT, fat emboli from bone fracture, air emboli

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14
Q

What is Congenital Heart Disease and what is it most commonly caused by?

A
  • abnormality of the Heart or Great Vessels due to sporadic genetic mutations or environmental toxins (fetal alcohol syndrome)
  • MOST COMMON structural birth defect with VSD (42%) and ASD (10%) being the most common forms
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15
Q

What does a child with Down’s Syndrome look like and what is the most common heart defect associated with them?

A

child: epicanthic folds and flat facial profile, simian crease of palm, umbilical hernia, gap between 1st/2nd toe
- MOST COMMON genetic cause of congenital heart disease

heart defect: atrioventricular defects or VSD

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16
Q

What heart defects would you see in pts. with:

  1. Marfan Syndrome (2)
  2. DiGeorge Syndrome (3)
  3. Turner Syndrome
  4. Patau (13) or Edwards (18) Syndromes (3)
A
  1. aortic aneurysm or dissection (Fibrillin-1 mutation)
    • also see mitral or aortic valve prolapse
  2. Conotruncal heart abnormalities, ASD, VSD
    • “CATCH 22” –> deletion of 22q11 (C = cardiac)
    • abnormal face, thymic aplasia, cleft palate, hypocal.
  3. coarctation of the aorta (45 XO female)
  4. PDA, VSD, ASD
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17
Q

What is the difference between a Left-Right Shunt and a Right-Left Shunt?

A

L–>R: high pressure left heart with low pressure right heart
- presents asymptomatically, no cyanosis

R–>L: blood bypasses pulmonary circulation

  • cyanosis, hypertrophic osteoarthropathy, “clubbing”
  • chronic hypoxia
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18
Q

What are 3 examples of Left to Right Shunts and what are 4 examples of Right to Left Shunts?

A

L–>R: VSD, ASD, PDA

R–>L: Tetralogy of Fallot, Transposition of the Great Arteries, Tricuspid Atresia, Truncus Arteriosus

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19
Q

What clinical increases are seen in VSD, ASD, and PDA?

What is a serious complication that can occur because of these conditions?

A

ASD/VSD = inc. right ventricle and pulmonary outflow volumes

PDA = inc. pulmonary blood flow, pulmonary pressure and hypertension

transient increases in right-sided pressure (cough) can cause paradoxical embolus to form do to connections to left heart

20
Q

Atrial Septal Defects

Where are Secundum, Primum, and Sinus Venosa defects located?

How does ASD typically present?

A

Secundum: center of atrial septum (90%)
Primum: adjacent to AV valves (5%)
Sinus Venosa: near entrance of Sup. Vena Cava
- anomalous pulmonary venous return

clinical: usually asymptomatic till after > 30 yo –> ejection systolic murmur (can be repaired)

21
Q

Ventricular Septal Defect

What is its most common form and how does it present clinically?

A
  • MOST COMMON congenital heart disease (90% are membranous VSD)
    clinical: HOLOSYSTOLIC murmur, large VSD = right ventricular hypertrophy, pulmonary HTN, SHUNT REVERSAL (cyanosis/death)
22
Q

What is Eisenmenger Syndrome (Shunt Reversal)?

A
  • occurs when a large Left-Right Shunt (VSD typically) causes increased Pulmonary Blood Flow, leading to endothelial dysfunction and irreversible vascular remodeling (THICKENED WALLS)
  • as pulmonary vessel walls thicken, pulmonary vascular resistance increases causing an INVERSION of the shunt (now RIGHT –> LEFT) preventing blood oxygenation from taking place
  • leads to CYANOSIS and DEATH
23
Q

What is a Patent Foramen Ovale?

What is a potential problem of disease?

A
  • open connection between Right and Left atrium that never closed (80% normally by 2 yrs)
  • flap can open if right side pressure increases, such as in bowel movements or coughing/sneezing
  • potential for paradoxical embolus to form, similar to ASD/VSD/PDA (embolus travels through open flap to left heart)
24
Q

What is Patent Ductus Arterious caused by (2) and what does it sound like on auscultation?

What does it cause clinically and what are two molecules that can keep it open or close it?

A
  • connection between pulmonary artery and aorta that fails to close due to HYPOXIA or inc. pulmonary vascular pressure (VSD)
    • initially left –> right and asymptomatic
  • produce harsh, MACHINE-LIKE MURMUR

clinical: large = inc. pulmonary pressure with shunt reversal –> CYANOSIS
- isolated: close with INDOMETHACIN
- preserve: keep open with PROSTAGLANDIN E

25
Q

What is Tetralogy of Fallot and what are its 4 principal features?

A
  • right to left shunt that cause cyanosis

PF: ventricular septal defect, right ventricular hypertrophy, pulmonary valve stenosis, OVERRIDING AORTA (centered at VSD, not left ventricle)

amount of stenosis dictates severity of condition

26
Q

How does Tetralogy of Fallot present clinically?

What is a “Tet” spell?

A
  • MOST COMMON congenital cyanotic heart disease (infants cyanotic from birth in most cases)
    clinical: VSD causes HOLOSYSTOLIC murmur, SYSTOLIC EJECTION murmur (pulmonary stenosis), compensatory squatting in children

Tet = cyanosis, syncope during emotional distress/excitement/inc. activity

children turn blue when crying or feeding

27
Q

What is an uncommon X-Ray finding that is indicative of Tetralogy of Fallot?

A

BOOT SHAPED HEART

  • see concave pulmonary segment with an upturned cardiac apex

most cases do NOT show this appearance though

28
Q

What is Transposition of the Great Arteries?

What is needed for pts to survive?

A
  • aorta and pulmonary artery are SWITCHED (pulmonary artery connects to left atrium and aorta connects to right atrium)
    • hypertrophic RV with thin LV
  • INCOMPATIBLE WITH LIFE unless shunt is present or induced, needs definitive surgery within the 1st month
    • Cyanosis and trouble breathing after birth

can keep PDA open with Prostaglandin E to help until surgery can be performed

29
Q

What is Tricuspid Atresia?

What is required to maintain oxygenation and what is the outlook of disease?

A
  • complete occlusion of the tricuspid valve that presents as severe, immediate cyanosis after birth
  • requires ASD and VSD to maintain oxygen, but even with surgery 90% of kids will die within the first decade
30
Q

What is Coarctation of the Aorta and what two vascular problems is it commonly seen with? (BA/BA)

What congenital condition is this commonly seen with?

What is a common imaging finding in patients with disease?

A
  • focal narrowing of the aorta (2x M) that can be seen with bicuspid aortic valve and berry aneurysm
    • females with Turner Syndrome (45 XO)
  • see RIB NOTCHING in longstanding adult form, due to pressure erosion
    • dilated, tortous collateral vessels develop
31
Q

Coarctation of the Aorta

What is the difference between Adult and Infantile forms?

A

A: has NO patent ductus arteriosus, usually no symptoms

  • hypertension in UE with hypotension of LE
  • cold LE and femoral pulse delay; Rib Notching

I: has Patent Ductus Arteriosus; presents at birth

  • cyanosis in lower half of body
  • absent femoral pulse; heart failure and shock
32
Q

What is Hypoplastic Left Heart Syndrome?

A
  • left ventricle is hypotrophic with aortic stenosis

- ASD with PDA provides blood in children with condition, but will require surgery once PDA closes

33
Q

What are the six classical features of Myocardial Infarction? (SCP/PR/WP/S/NV/DD)

A
  1. prolonged substernal chest pain (> 30 min)
    • “crushing, stabbing, squeezing”
  2. pain radiates to jaw, neck, shoulder
  3. rapid, weak pulse
  4. profuse sweating
  5. nausea and vomiting
  6. dyspnea and discomfort
34
Q

When does irreversible cell injury occur in Myocardial Infarction?

A

occurs in the first 20-40 minutes

“time is myocardium” = treating early saves the heart from inc. damage

35
Q

What are the specific biomarkers used to track Myocardial Infarction?

A
  • most sensitive and specific markers are cardiac-specific proteins Troponin T and I (cTnT and cTnI)
  • can also track creatinine kinase, specifically MB heterodimers (principally in cardiac muscle) but are also found in many other areas (sensitive but not specific) –> CKMB
  • myoglobin has been replaced by troponin studies
36
Q

When do cardiac markers first start to elevate and how long does it take them to normalize?

A
  • CKMB, cTnT, and cTnI elevate within 3-12 hrs with peak of CKMB and cTnI at 24 hrs

CKMB is back to normal in 48-72 hrs
- can be used to assess for re-infarct after initial attack

cTnI/cTnT are back to normal after 5 days

person can present acutely before enzymes are elevated, so check serial troponins

37
Q

Where do Transmural Infarcts occur when permanent occlusion occurs to:

  1. Left Anterior Descending A.
  2. Left Circumflex A.
  3. Right Coronary A.
A
  1. most common site of infarction (“Widow Maker”)
    • affects Apex, anterior LV, and anterior 2/3 of septum
  2. affects lateral wall of LV
  3. second most common site of infarction
    • affects RV, posterior LV wall, posterior 1/3 of septum
38
Q

What are 3 ways that Subendothelial Infarcts can arise?

A
  • can occur after reperfusion of transmural infarct (REGIONAL)
  • can occur due to global hypotension (CIRCUMFERENTIAL)
  • can ALSO occur with microinfarcts due to small intramural vessel occlusion due to embolic disease or DRUG USE (cocaine)
39
Q

Morphologic Evolution of Myocardial Infarction

What is seen at:

  1. 30 min - 4 hrs
  2. 4-12 hrs
  3. 12-24 hrs
  4. 1-3 days
  5. 3-7 days
  6. 7-10 days
  7. 10-14 days
  8. 2-8 wks
  9. > 2 months
A
  1. wavy fibers due to pulling of viable fibers on dead ones
  2. dark mottling; edema first appears; coag. necrosis
  3. dark mottling; nuclei pyknosis; myocyte hypereosinophilia
  4. yellow-tan infarct; loss of nuclei w/coagulative necrosis; acute neutrophil infiltrate
  5. hyperemic border; myofibers disintegrate; MOs
  6. max yellow; depressed red margins; granulation tissue at margins
  7. red-gray infarct borders; granulation tissue and collagen deposition; new BV
  8. gray-white scar; inc. collagen w/dec. cellularity; fibroblasts replace myocytes
  9. scarring complete w/dense collagenous scar
40
Q

What is the 1st sign of irreversible injury in Myocardial Infarction?

A

WAVY FIBERS

  • due to viable fibers pulling on dead fibers that causes twisting
41
Q

What are early (first 24 hr) complications of Myocardial Infarction? (A/CD)

A
  1. Arrhythmias - NUMBER 1 cause of death
    • ventricular fibrillation
    • 1/2 of deaths occur within 1 hour of onset
  2. Contractile Dysfunction
    • depends on size of infarct and loss of function
    • leads to CARDIOGENIC SHOCK
42
Q

What are intermediate (2-4+ day) complications of Myocardial Infarction? (R/AP)

What are risk factors for myocardial rupture? (A/MI/LVH)

A
  1. Septal, Free Wall, and Papillary Rupture
    • can cause valve incompetence
    • papillary rupture = most common mechanical problem of MI (typically due to RCA occlusion)
  2. Acute Pericarditis
    • requires transmural infarct 2-4 days post MI (FATAL)
    • can lead to acute pericardial tamponade
    • RF: inc. age, first MI, no LV hypertrophy
43
Q

What are late (>2 wk) complications of Myocardial Infarction? (4)

A
  1. Dressler Syndrome (chronic pericarditis)
    • fibrinous pericarditis due to Abs to myocardial proteins in blood
    • fever, pleuritic pain, pericardial effusion
  2. Ventricular Aneurysm
    • after large transmural infarct w/expansion
  3. Life-threatening Arrhythmias (due to remodeling)
  4. Progressive Congestive Heart Failure
44
Q

What is Angina and what are its 3 types?

A
  • transient, often recurrent chest pain induced by myocardial ischemia INSUFFICIENT to induce myocardial infarction
    types: Stable, Prinzmetal, and Unstable
45
Q

Stable Angina vs Prinzmetal Angina

A

SA: stenotic occlusion of coronary artery

  • can oxygenate at rest but not during exercise
  • substernal pressure, squeezing, burning

PA: episodic coronary artery spasm

  • 3-6 mo clusters of attack with asymptomatic periods
  • unrelated to physical activity, HR, or BP

both can be relieved with vasodilators

46
Q

What is the difference between Ruptured and Progressive Unstable Angina?

A

R: due to ruptured plaque with non-occlusive thrombus
- acute chest pain, felt w/activity AND REST

P: due to progressive mechanical obstruction

  • “crescendoing” angina = worsening pain over time
  • should NOT occur at rest
47
Q

What is the difference in ECG and troponins for:

  1. Stable Angina
  2. Unstable Angina
  3. NSTEMI
  4. STEMI
A
  1. normal ECG, normal troponin lvls
    • demand ischemia, no infarct
  2. normal, inverted T waves, or ST depression
    • NORMAL troponin lvls
    • supply ischemia, no infarct
  3. normal, inverted T waves, or ST depression
    • ELEVATED troponin lvls
    • subendocardial infarct
  4. hyperactive T waves or ST elevation
    • elevated troponin lvls
    • transmural infarct

CPR II Exam 1 (15 decks)

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