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CPR Exam 1 > Cardio Pathology Part 1 > Flashcards

Cardio Pathology Part 1 Flashcards

1
Q

How is dominance of the heart defined?

A

Defined due to the preference of the posterior descending artery

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2
Q

What happens as the heart ages?

A

There is a reduction in compliance and elasticity

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3
Q

What can happen to the mitral valve as the heart ages?

A

Become fibrous which will cause a buckling prolapse during systole leading to atrial dilation and arrhythmia

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4
Q

What do calcific deposits on the valves cause?

A

Aortic stenosis

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5
Q

How do the chambers of the heart change with age?

A
  • Left ventricle cavity size reduced (esp in HTN)

- Atrial dilation

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6
Q

What atherosclerotic changes occur with age?

A
  • Significant stenosis (MI, aortic dissection)
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7
Q

What epicardial and myocardial changes occur with age?

A
  • Increase in epicardial fat
  • Lipofuscin accumulates
  • Basophilic degeneration
  • Myocyte loss
  • Amyloid deposition (transthyretin)
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8
Q

What are the two types of pump failure in cardiovascular dysfunction?

A
  • Inadequate contraction (systole)

- Inadequate filling (diastole)

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9
Q

What does flow obstruction cause?

A
  • Increase in resistance pressure (HTN, valve stenosis)

- Decreased blood flow (atherosclerosis; cardiac ischemia)

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10
Q

What causes regurgitant flow?

A
  • Incompetent valve (valvular disease)
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11
Q

What causes shunted flow?

A
  • Congenital disease (VSD, PDA)

- After MI

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12
Q

What can cause cardiac conduction abnormalities?

A
  • Ischemic injury (infarction, direct nodal injury, dilated dysfunction)
  • Heritable arrhythmias
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13
Q

What can cause vessel rupture?

A
  • Aortic dissection

- Trauma (car crash from hitting chest on steering wheel)

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14
Q

What is a good approximation of heart weight?

A
  • 0.5% of BW
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15
Q

What is the definition of dilation?

A

Enlarged chamber size

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16
Q

What is the definition of hypertrophy?

A
  • Increase in muscle mass or thickening of heart muscle (due to cardiomyocyte size or length)
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17
Q

What is cardiomegaly?

A
  • Abnormal enlargement of the heart (increase in weight or size)
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18
Q

What are some causes of hypertrophy or dilation? What causes this?

A
  • HTN, Vascular disease, and MI

- Caused by increased cardiac work

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19
Q

What causes congestive heart failure?

A
  • A pump failure which causes inadequate blood supply to the body
  • Either a systolic dysfunction or a diastolic dysfunction)
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20
Q

What are some causes of systolic dysfunction?

A
  • Decreased ejection fraction
  • Ischemic injury
  • Dilated cardiomyopathy
  • Valve regurgitation
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21
Q

What are some causes of diastolic dysfunction?

A
  • Will have normal EF but lower total volume due to less filling
  • HTN
  • Aortic stenosis
  • Hypertrophic cardiomyopathy
  • Fibrosis
  • Restrictive cardiomyopathy
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22
Q

What are some primary causes of left sided CHF?

A
  • MI
  • HTN
  • Left-sided valve disease
  • Primary myocardial disease
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23
Q

What are the clinical effects of left sided CHF?

A
  • Pulmonary congestion/edema

- Decreased tissue perfusion (decreased cerebral perfusion and decreased renal perfusion, azotemia)

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24
Q

What is seen on CXR in a patient with left sided CHF?

A
  • Kerley B lines (like in pneumonia)
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25
Q

What is seen histologically in a patient with left sided CHF?

A
  • Hemosiderin-laden macrophages
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26
Q

What is the most common cause of right sided CHF?

A
  • Left sided failure
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27
Q

Why is left sided heart failure the number one cause of right sided failure?

A
  • Increase in pulmonary pressure causes the right side to fail
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28
Q

What is isolated right heart failure called?

A
  • Cor Pulmonale
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29
Q

What are some causes of pulmonary HTN?

A
  • Parenchymal lung diseases (most common)
  • Lung thromboemboli
  • Primary pulmonary HTN (Rare)
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30
Q

What are some clinical effects due to venous congestion?

A
  • Hepatosplenomegaly
  • Distended jugular veins
  • Effusions of peritoneal, pleural, and pericardial spaces
  • Edema (esp ankles)
  • Nutmeg liver
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31
Q

What are some causes of congenital heart disease?

A
  • Sporadic genetic mutations (common)

- Environmental toxins (fetal alcohol syndrome)

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32
Q

What is the most common congenital heart defect in those with down syndrome?

A
  • Atrioventricular or ventricular septal defects
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33
Q

What is the most common congenital heart defect in those with marfan syndrome?

A
  • Aortic aneurysm/dissection
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34
Q

What is the mnemonic for DiGeorge Syndrome?

A
  • CATCH-22
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35
Q

What are the most common congenital heart defects in those with DiGeorge syndrome?

A
  • Conotruncal heart abnormalities
  • ASD
  • VSD
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36
Q

What is the most common congenital heart defect in those with Turner’s syndrome?

A
  • Coarctation of the aorta
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37
Q

What are the most common congenital heart defects in those with Patau’s or Edward’s syndromes?

A
  • PDA
  • VSD
  • ASD
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38
Q

What are the two types of cardiac shunts?

A
  • L to R

- R to L

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39
Q

What causes a left to right cardiac shunt?

A
  • High pressure in the left heart and lower pressure in the right heart
  • Could also be seen in aorta to pulmonary trunk due to PDA
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40
Q

What does a person with a left to right shunt present with clinically? Why?

A
  • Asymptomatically with no cyanosis

- This is due to the higher pressure side being oxygenated

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41
Q

What are the different defects that cause a left to right shunt?

A
  • ASD
  • VSD
  • PDA
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42
Q

What causes a right to left cardiac shunt?

A
  • When blood bypasses the pulmonary circulation
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43
Q

What does a person with a right to left shunt present with clinically?

A
  • Symptomatic with cyanosis
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44
Q

What are the different defects that cause a right to left shunt?

A
  • Tetralogy of Fallot
  • Transposition of the great vessels
  • Tricuspid atresia
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45
Q

What can arise if there is a shunt reversal in a normally left to right shunt?

A
  • Paradoxical embolus
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46
Q

How do an ASD and VSD specifically cause a left to right shunt?

A
  • They increase the right ventricular and pulmonary outflow volumes
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47
Q

How does a PDA specifically cause a left to right shunt?

A
  • Increases pulmonary blood flow, pulmonary pressure, and HTN
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48
Q

What are the types of ASD?

A
  • Secundum ASD
  • Primum anomaly
  • Sinus venosa defect
49
Q

What is a secundum ASD?

A
  • 90% of all ASD cases

- Located in the center of the septum

50
Q

What is a primum anomaly?

A
  • 5% of all ASD cases
  • Located adjacent to the AV valves
  • Associated with AV valve abnormalities and/or VSD
51
Q

What is a sinus venosa defect?

A
  • 5% of all ASD cases
  • Located near the entrance of the SVC
  • Associated with anomalous pulmonary venous return
52
Q

What is the clinical features of ASD’s?

A
  • Usually asymptomatic until adulthood when it causes an ejection systolic murmur
  • Mortality is low
53
Q

What is the most common form of congenital heart disease?

A
  • VSD (90% are membranous)
54
Q

What are the clinical aspects of a VSD?

A
  • Cause a holosystolic murmur

- Effects depend on size and presence of other heart defects

55
Q

What can large VSD shunting lead to?

A
  • Right ventricular hypertrophy, heart dysfunction
  • Pulmonary hypertension
  • Unclosed VSD could lead to a shunt reversal causing cyanosis and death
56
Q

What is the shunt reversal process called?

A
  • Eisenmenger syndrome
57
Q

What is the pathogenesis of Eisenmenger syndrome?

A
  • A left to right shunt has an increase in pulmonary blood flow
  • Irreversible endothelial dysfunction and pulmonary vascular remodeling occurs
  • The increase in vascular resistance causes an inverted shunt
58
Q

What are some problems with patients that have a patent foramen ovale?

A
  • 20% do not close and the flap can open if the right sided pressure is increased
  • Even a slight increase in pressure can cause a R-L shunt
59
Q

What are some examples that increase the right sided pressure in a patent foramen ovale?

A
  • Valsalva, bowel movements, coughing/sneezing
60
Q

What could happen in a patent foramen ovale?

A
  • Paradoxical embolus
61
Q

What are some reasons that a patent ductus arteriosus will fail to close?

A
  • If an infant is hypoxic or have defects with increased pulmonary vascular pressure
62
Q

What kind of murmur is produced with a PDA?

A
  • Machinery like murmur
63
Q

How does a PDA present in a patient?

A
  • Usually asymptomatic at birth

- Have a left to right shunt and usually no cyanosis

64
Q

What can help close an isolated PDA?

A
  • Indomethacin
65
Q

What can be given to keep a PDA patent? Why would we do this?

A
  • PGE is given to preserve PDA

- Can be lifesaving in certain congenital malformation

66
Q

What are the four principal features of Tetralogy of Fallot?

A
  • VSD
  • Right ventricular hypertrophy
  • Pulmonary valve stenosis
  • Overriding aorta
67
Q

What are “tet” spells?

A
  • Cyanosis

- Syncope during emotional distress, excitement, or increased activity

68
Q

What should you look for in someone with Tetralogy of Fallot?

A
  • Infants will be cyanotic at birth
  • Tet spells
  • Compensatory squatting in children to relieve symptoms
  • Boot shaped heart on CXR
69
Q

What occurs in the transposition of the great arteries?

A
  • Aorta and pulmonary artery are switched
70
Q

What is expected at birth in an infant with tetralogy of fallot?

A
  • Cyanosis

- Incompatible with life unless there is a shunt in place (VSD, PDA, PFO)

71
Q

What is tricuspid atresia?

A
  • Complete occlusion of the tricuspid valve
72
Q

How is oxygenation maintained in tricuspid atresia?

A
  • By a shunt like ASD/PFO AND a VSD
73
Q

What is expected at birth in an infant with tricuspid atresia?

A
  • Severe, immediate cyanosis with a high mortality rate
74
Q

What is coarctation of the aorta?

A
  • Focal narrowing of the aorta
75
Q

Who is most likely to present with coarctation of the aorta?

A
  • Most common in male

- But also seen sometimes in Turner’s syndrome

76
Q

What other pathologies are seen with coarctation of the aorta?

A
  • Bicuspid atresia

- Berry aneurysm

77
Q

What is seen in the infantile form of coarctation of the aorta?

A
  • PDA is seen
  • Infant will have cyanosis of their lower half
  • Absent femoral pulses
  • May have heart failure and shock
78
Q

What is seen in the adult form of coarctation of the aorta?

A
  • PDA is absent
  • Usually asymptomatic but there will be HTN in UE and hypotension in LE
  • LE will be cold and femoral pulse delay
  • May see concentric LV hypertrophy and dysfunction
79
Q

Where does coarctation of the aorta occur in infants? Adults?

A
  • Infants: before or on PDA

- Adults: after ligamentum arteriosum

80
Q

What does mild aortic stenosis cause?

A
  • LV hypertrophy
81
Q

Where is aortic stenosis seen?

A
  • In hypoplastic left heart syndrome

- ASD with PDA provides blood

82
Q

What is seen in pulmonary stenosis?

A
  • Mild, isolated stenosis or part of tetralogy of fallot/transposition of great arteries
83
Q

What is the leading cause of death in US?

A
  • Ischemic heart disease
84
Q

What increases the risk of coronary artery disease?

A
  • Age
  • Male gender
  • Postmenopausal women
85
Q

What are some causes of ischemic heart disease?

A
  • Atherosclerosis
  • Coronary artery emboli
  • Myocardial vessel inflammation
  • Vessel spasm
86
Q

What are the clinical features of ischemic heart disease?

A
  • Prolonged substernal chest pain (crushing, stabbing, squeezing)
  • Radiates to neck, shoulder, or jaw
  • Rapid, weak pulse
  • Profuse sweating
  • Nausea and vomiting
  • Dyspnea and discomfort
87
Q

What is the earliest a biomarker for ischemic heart disease?

A
  • CKMB is the earliest at 3 hours
88
Q

When does the CKMB biomarker normalize?

A
  • 48-72 hours
89
Q

when do the cTnI and cTnT biomarkers normalize?

A
  • > 5 days
90
Q

What is the best biomarker used to look at MI?

A
  • Troponin I (most sensitive and specific)
91
Q

If the LAD gets occluded, what section of the heart is affected?

A
  • Apex
  • LV anterior wall
  • Anterior 2/3 of septum
92
Q

If the left circumflex gets occluded, what section of the heart is affected?

A
  • LV lateral wall
93
Q

If the right coronary artery gets occluded, what section of the heart is affected?

A
  • RV free wall
  • LV posterior wall
  • Posterior 1/3 of septum
94
Q

What is the pathway of necrosis in myocytes after an MI?

A
  • Necrosis occurs from inside to outside (it starts furthest away from the vessels)
95
Q

What happens on day 1 after an MI?

A
  • Coagulative necrosis occurs presenting with wavy fibers on histo, some neutrophils present
  • Life threatening arrhythmias present
  • Cardiogenic shock occurs due to contractile dysfunction
96
Q

What happens on day 3 after an MI?

A
  • A yellow infarct necrosis, hyperemic border is present on gross exam
  • Marked acute neutrophilic inflammatory infiltrate on histo
97
Q

What happens on days 3-7 after an MI?

A
  • Macrophages become more prominent to get rid of necrosed tissue
  • Mitral regurgitation occurs due to ischemic papillary muscles
  • Papillary muscle, ventricular septal wall, and left ventricular wall could all rupture
  • Acute pericarditis
98
Q

What happens 1-2 weeks after an MI?

A
  • Some granulation tissue has formed with some deposition of collagen
  • Chronic pericarditis occurs due to autoimmune reaction towards myocardial proteins released into blood (Dressler syndrome)
  • Life threatening arrhythmias occur due to remodeling of myocardium
99
Q

What happens 2 months after an MI?

A
  • Scarring with dense fibrosis is seen on histo
100
Q

What are some risk factors for a myocardial rupture?

A
  • Increased age
  • First MI
  • Absence of LV hypertrophy
101
Q

What does a myocardial rupture cause?

A
  • Acute pericardial tamponade
102
Q

Who is a myocardial rupture most likely seen in?

A
  • Elderly due to decreased muscle mass
103
Q

What is Dressler Syndrome?

A
  • An autoimmune reaction to myocardial proteins in the blood
104
Q

What does dressler syndrome present with?

A
  • Fever
  • Pleuritic pain
  • Pericardial effusion
105
Q

What is a ventricular aneurysm?

A
  • Occurs after a large transmural infarct with expansion

- There is a thin walled scar which causes the aneurysm

106
Q

What is angina pectoris?

A
  • A transient, often recurrent chest pain
107
Q

What induces the chest pain in angina pectoris?

A
  • Myocardial ischemia but not enough to induce an MI
108
Q

What are the three variants of angina pectoris?

A
  • Stable angina
  • Prinzmetal angina
  • Unstable angina
109
Q

What is stable angina?

A
  • A stenotic occlusion of the coronary artery
110
Q

What is the presentation of stable angina?

A
  • Substernal pressure
  • Squeezing
  • Burning
111
Q

What relieves the symptoms of stable angina?

A
  • Rest

- Vasodilators

112
Q

What induces stable angina?

A
  • Physical activity

- Stress

113
Q

What is prinzmetal angina?

A
  • Episodic coronary artery spasm
114
Q

What relieves the symptoms of prinzmetal angina?

A
  • Vasodilators
115
Q

Is prinzmetal angina related to physical activity, HR, or BP?

A

No

116
Q

What is unstable angina?

A
  • Caused by rupture of athersclerotic plaques with partial thrombus
117
Q

What is the presentation of someone with unstable angina?

A
  • Present at rest

- Has a crescendo pattern of increasing duration or severity

118
Q

What should be assumed if someone presents with sudden onset of dyspnea, SOB, crushing, stabbing, or squeezing chest pain that radiates to the jaw?

A

Transmural acute MI

CPR Exam 1 (21 decks)

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