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CPR 2 Exam 1 > Cardiac Pathology 1 > Flashcards

Cardiac Pathology 1 Flashcards

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1
Q

What are the major branches that feed the heart?

A

Left anterior descending artery
Left circumflex artery
Right coronary artery

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2
Q

What artery does the left descending artery and left circumflex artery arise from?

A

Left coronary artery

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3
Q

Which artery is the most common site of critical stenosis?

A

Left anterior descending artery

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4
Q

What is the most common dominant heart?

A

Right dominant

Right coronary artery supplies posterior aspect of the heart

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5
Q

What supplies a codominant heart?

A

Left circumflex artery

Right coronary artery

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6
Q

What happens to compliance and elasticity as we age?

A 
Decreased compliance
Decreased elasticity (due to increased collagen)
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7
Q

Fibrosis of the mitral valve causes what?

A

Buckling into left atrium -> atrial dilation -> atrial fibrillation

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8
Q

Calcification of the aortic valve leads to what?

A

Aortic stenosis -> increased left ventricular pressure -> hypertrophy -> heart failure

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9
Q

What is lambl’s excrescences?

A

Filiform fronds that occur at sites of valvular closure

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10
Q

How do Lambl’s excrescences form?

A

Small thrombi which form from minor endothelial damage due to wear and tear

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11
Q

What cavity decreases size in the aging heart?

A

Left ventricle (usually due to HTN)

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12
Q

What cavity increases in size with the aging heart?

A

Atrial dilation (due to fibrous mitral valve)

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13
Q

Atherosclerosis affecting the vasa vasorum causes what?

A

Predisposition to dissection

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14
Q

What are epicardial and myocardial changes seen in the aging heart?

A 
Increased epicardial fat
Lipofuscin accumulates
Basophilic degeneration
Myocyte loss
Amyloid deposition
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15
Q

What is the function of epicardial fat?

A

Mechanically cushion cardiac vessels during myocardial contraction

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16
Q

What is lipofuscin?

A

Yellow-brown pigment which is a product of intracellular catabolism and oxidant stress

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17
Q

Where does lipofuscin accumulate?

A

Liver
Kidney
Ganglion cells
Heart

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18
Q

What is transthyretin?

A

Normal serum protein that binds and transports thyroxine

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19
Q

What is senile cardiac amyloidosis?

A

Amyloid deposition that causes stiffness and thickening of the walls leading to SOB, exercise intolerance, and heart failure

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20
Q

What is pump failure?

A

Insufficient contraction during systole to push blood into circulation
OR
Insufficient filling of blood into the heart during diastole

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21
Q

What does flow obstruction cause?

A

Increase the resistance pressure that the heart has to push against (valve stenosis, HTN)
Ischemic myocyte loss (atherosclerosis, cardiac ischemia)

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22
Q

What is valvular regurgitation?

A

Valve is incompetent

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23
Q

What can valvular regurgitation cause?

A

Volume overload of previous heart chamber
Dilating the heart
Decreasing its ability to adequately pump

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24
Q

What is shunted blood flow?

A

Blood flows between two structures which are not commonly connected

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25
When is shunting of blood seen?
VSD PDA After MI
26
What is the most common cause of death in the first 24 hours after infarction?
Arrhythmias
27
How does ischemic injury cause arrhythmias?
Ischemic injury -> cardiac remodeling -> increased fibrosis -> dilated cardiac dysfunction -> arrhythmias
28
When does traumatic aortic dissection frequently occur?
MVC
29
What happens with aortic dissection due to MVC?
Rapid deceleration forces causes blow to the chest as the steering wheel impacts the driver -> traumatic separation of ligmentum arteriosum from aorta
30
When does abnormal dilation of a heart chamber occur?
Volume overload
31
When does hypertrophy occur?
Increase in pressure
32
Increased pressure causes what type of hypertrophy?
Concentric
33
Increased volume causes what type of hypertrophy?
Eccentric
34
In dilated hearts how is hypertrophy measured?
Heart weight
35
What happens to myocytes in concentric hypertrophy?
Increase in size or diameter of myocytes
36
What happens to myocytes in eccentric hypertrophy?
Increase in length
37
What causes left ventricular hypertrophy?
Chronic HTN | Aortic valvular stenosis
38
Overload of what causes cardiac dysfunction and heart failure?
Pressure | Volume
39
Is there an increase in capillary number with pathologic hypertrophy?
No
40
Is there an increase in capillary number in exercise induced hypertrophy?
Yes
41
Why does hypertrophy lead to ischemic decompensation
No additional capillaries but increased oxygen required
42
What happens with increased activity of the neurohumoral system?
Norepinephrine increases contractility in an attempt to maintain systemic perfusion but ultimately the increase in heart rate and contractility can't keep up with peripheral demand
43
What is the most common endpoint for cardiovascular disease?
Congestive heart failure
44
What is diastolic congestive heart failure?
Blood does not adequately fill the ventricle causing less blood to pump into circulation
45
When does diastolic congestive heart failure occur?
Ventricles are too thick or stiff
46
What is systolic congestive heart failure?
Inadequate contractile strength to pump an adequate amount of blood out of the heart
47
When does systolic congestive heart failure occur?
Dilated cardiac dysfunction
48
Which heart failure has decreased ejection fraction?
Systolic
49
What is ejection fraction?
Total amount of blood ejected from the heart
50
Why doesn't the heart pump well in systolic congestive heart failure?
Ischemic injury removes cardiomyocytes Ventricles are too dilated to pump well (dilated cardiac dysfunction) Valve regurgitation distends the pump causes it to be ineffective
51
Which heart failure has normal ejection fraction?
Diastolic
52
What leads to diastolic dysfunction?
``` HTN Aortic stenosis Hypertrophic cardiomyopathy Fibrosis Restrictive cardiomyopathy ```
53
What can causes myocardial fibrosis?
Radiation therapy | Amyloid deposition
54
What is the pathophysiology of left heart failure?
Heart unable to pump blood from the left ventricle to the systemic circulation results in backup of fluid into the pulmonary circulation and lungs Decreased cardiac output and tissue perfusion (forward failure) Pooling of blood backward (backward failure)
55
What are the main causes of left heart failure?
Myocardial ischemia HTN Left-sided valve disease Myocardial disease
56
What are the symptoms of left sided heart failure?
``` Pulmonary congestion/edema Cough Dyspnea SOB Wheezing Crackles in lungs Cough Orthopnea (dyspnea when laying flat) ```
57
What is paroxysmal nocturnal dyspnea?
Dyspnea at night awaking them from sleep
58
Why does paroxysmal nocturnal dyspnea occur?
Respiratory and cough center response is blunted during sleep (feels like they are suffocating)
59
Impaired left ventricular function in left heart failure can cause what?
Atrial dilation leads to atrial fibrillation
60
Loss of atrial function in atrial dilation and atrial fibrillation leads to what?
Pump failure
61
Lack of perfusion to the brain in left heart failure leads to what?
Restlessness Confusion Ischemic cerebral injury Coma
62
Lack of perfusion to the kidneys in left heart failure leads to what?
Azotemia Increased creatinine Increased BUN
63
What edema is seen with left heart failure?
Perivascular | Interstital edema
64
What is seen on CXR with left heart failure?
Kerley B lines
65
What are Kerley B lines?
Short parallel lines that reach the lung periphery | Manifestation of interstitial pulmonary edema (specifically interlobular septa)
66
What other conditions are Kerley B lines seen in?
Lymphangitis carcinomatosis Lymphoma Pneumonia
67
What do RBCs do in left heart failure?
Extravasate into edema within alveolar spaces
68
What are the histologic signs of heart failure?
Hermosiderin-laden macrophages (due to extravasated RBCs)
69
What is the most common cause of right heart failure?
Left heart failure
70
Why does left heart failure cause right heart failure?
Backpooling of blood from the left heart into the pulmonary vasculature which increases the pressure gradient that the right ventricle has to pump against
71
Where does the blood pool up in right heart failure?
Right atrium | Venous system
72
What happens to the liver in right heart failure?
Impaired hepatic venous draining leading to stasis of blood in the hepatic parenchyma and hepatomegaly
73
What happens to the spleen in right heart failure?
Impaired splenic vein draining
74
Peritoneal, pleural, and pericardial effusions develop in what type of heart failure?
Right heart failure
75
Why does peritoneal, pleural, and pericardial effusions develop in right heart failure?
Intravascular pressure is high, displacing fluid into mesothelial lined body cavities
76
Marked weight gain is seen in which type of heart failure?
Right heart failure
77
What is the pathophysiology of isolated right sided heart failure?
With pulmonary HTN the right ventricle pushes against an increased pressure gradient, when the pressure is more than the pump can counter the right heart fails and fluid backs up into venous circulation
78
What is cor pulmonale?
Isolated right-sided heart failure
79
What are three causes of pulmonary HTN that can leads to isolated right heart failure?
1) Parenchymal lung disease 2) Lung thromboemboli 3) Primary pulmonary hypertension
80
Liver and splenic congestion leads to what in right heart failure?
Hepatosplenomegaly
81
What are the symptoms of right heart failure?
``` Distended jugular veins Effusions Edema (gravity dependent) Weight gain Ascites Fatigue Exertional dyspnsea ```
82
Nutmeg liver is common what type of heart failure?
Right sided heart failure
83
What liver hemorrhage is seen with right sided heart failure?
Centrilobular hemorrhage and necrosis
84
What is emphysema?
Chronic pulmonary parenchymal disease
85
Emphysema causes what cardiac conditions?
Pulmonary HTN | Right heart failure
86
What does the heart look like with cor pulmonale?
Hypertrophy of right ventricle | Normal left ventricle
87
Thromboemboli from DVTs can also cause what type of heart failure?
Right heart failure
88
What is acute cor pulmonale typically attributable to?
Large thromboembolus | Multiple thromboemboli in the pulmonary trunk
89
Thromboemboli in addition to right heart failure causes what?
Concomitant decreased systemic and coronary perfusion
90
What does the majority of congenital heart diseases arise from?
Faulty embryogenesis due to sporadic genetic abnormalities
91
Fetal alcohol syndrome causes what heart defect?
Septal defects
92
What is the most common cardiac abnormality?
VSD
93
What is the most common genetic cause of congenital heart disease?
Trisomy 21 (Down Syndrome)
94
What symptoms do patients with Down Syndrome have?
``` Epicanthic folds Flat facial profile Simian crease Mental retardation Abundant neck skin Intestinal stenosis Umbilical hernia Predisposition to leukemia Hypotonia ```
95
What is the most common heart defect with trisomy 21?
VSD
96
What heart defects are common with Marfan syndrome?
Aortic aneurysm Aortic dissection Mitral valve prolapse Aortic valve prolapse
97
DiGeorge syndrome is caused by a deletion in which chromosome?
22
98
What is the CATCH-22 acronym?
``` Cardiac abnormality Abnormal facies Thymic aplasia Cleft palate Hypocalcemia ```
99
What cardiac abnormality is associated with DiGeorge syndrome?
Conotruncal abnormalities
100
Conotruncal abnormalities occur in which heart field?
2nd
101
What are the conotruncal abnormalities?
Tetralogy of fallot | Transposition of great arteries
102
Turner syndrome is associated with which cardiac abnormality?
Coarctation of the aorta
103
Trisomy 13 (Patau syndrome) is associated with which cardiac abnormalities?
PDA | Septal defects
104
Trisomy 18 (Edward's syndrome) is associated with which cardiac abnormalities?
PDA | Septal defects
105
What are the two categories of shunts?
Left-to-right shunts | Right-to-left shunts
106
Which side of the heart has higher pressure?
Left side
107
What are the symptoms of left to right shunts?
Asymptomatic
108
What are the symptoms of right to left shunts?
Hypoxemia | Cyanosis
109
What does chronic hypoxemia cause?
Polycythemia
110
What is hypertrophic osteoarthropathy?
Inflammation of the periosteum of the connective tissue surrounding bone
111
What causes hypertrophic osteoarthropathy?
Long standing cyanosis
112
What shunt causing clubbing of tips of finger and toes?
Right-to-left
113
What are the left-to-right shunts?
ASD VSD PDA
114
What are the right-to-left shunts?
``` Tetrology of Fallot Transposition of the Great Arteries Tricuspid atresia Truncus arteriosus Coarctation of the aorta with PDA ```
115
What is the pathophysiology behind hypertrophic osteoarthropathy?
Megakaryocyte fragments bypass the lungs and release bradykinin, TGF-Beta1, VEGF, and PDGF causing clubbing, periostitis
116
All left-to-right shunts cause what?
Pulmonary HTN as increased blood increases the pressure in the pulmonary trunk
117
ASD and VSD causes increase in which volumes?
Right ventricles | Pulmonary outflow
118
PDA causes increase in what volume?
Increase pulmonary blood flow
119
What happens in a paradoxical embolism?
Venous embolus crosses to the arterial side (need a defect in the heart or major vessels)
120
What are the types of emboli?
Thromboemboli Septic emboli Traumatic bone marrow emboli Iatrogenic air emboli
121
What is the most common ASD?
Secundum (found in the center of the atrial septum)
122
What are the symptoms of ASD?
Usually asymptomatic (sometimes pulmonary HTN)
123
How are ASDs fixed?
Noninvasive endovascular approach
124
What are the two other common ASDs?
``` Primum anomaly (adjacent to AV valves) Sinus venosa (near entrance to SVC) ```
125
What is primum anomaly associated with?
AV valve abnormalities | VSD
126
What is sinus venosa defects associated with?
Anomalous pulmonary venous return
127
What murmur can be seen with ASDs?
Ejection systolic murmur
128
What is the most common congenital cardiac malformation?
VSD
129
Majority of VSDs involve what?
Membraneous interventricular septum
130
What are the other types of VSDs?
Subpulmonary (infundibular) AV canal Muscular
131
What are the symptoms of VSDs?
Asymptomatic except those associated with tetralogy of fallot
132
What murmur is seen with VSDs?
Holosystolic murmur
133
Do VSDs close spontaneously?
Yes
134
What are the symptoms of large VSDs?
Right ventricular hypertrophy Pulmonary HTN Shunt reversal -> cyanosis -> death
135
What is the Eisenmenger Syndrome?
Shunt reversal in a VSD
136
What pathway for Eisenmenger syndrome?
Long standing left to right shunt -> increased pulmonary blood flow -> endothelial dysfunction and pulmonary vascular remodeling -> increased in pulmonary vascular resistance -> inverted (right-to-left) shunt
137
Eisenmenger is associated with what?
Large VSDs
138
What is the endothelial damage done in Eisenmenger syndrome?
Arteriolar intimal proliferation Medial hypertrophy Capillary and arteriolar occlusion
139
Is endothelial damage in Eisenmenger syndrome reversible or irreversible?
Irreversible
140
What are the two natural shunts in the fetal circulation that bypass the lungs?
Foramen ovale | Ductus arteriosus
141
What does the foramen ovale connect?
Atria of the heart
142
What keeps the foramen ovale shut after birth?
Increased left sided heart pressure
143
What causes the patent foramen ovale to open?
Increased right heart pressure Valsalva Bowel movement Coughing/sneezing
144
Opening of a patent foramen ovale causes what?
Right-to-left shunting
145
What is clinically significant about a patent foramen ovale?
Possible paradoxical embolus
146
What does the ductus arteriosus connect?
Pulmonary artery and aorta
147
When does the ductus arteriosus typically close?
2-3 days after birth
148
What causes the ductus arteriosus not to close?
Hypoxia | Increased vascular pressure
149
What murmur is heard with patent ductus arteriosus?
Harsh, continuous medium pitched murmur with machine-like quality
150
What is used to close a patent ductus arteriosus?
Indomethacin
151
What shunt occurs with patent ductus arteriosus?
Left-to-Right
152
What can happen with a large patent ductus arteriosus?
Increased pulmonary pressure | Shunt reversal -> Cyanosis
153
What is used to preserve the patency of ductus arteriosus in certain congenital malformation?
Prostaglandin E
154
What are the four features of tetralogy of fallot?
1) VSD 2) Right ventricular hypertrophy 3) Pulmonary valve stenosis 4) Overriding aorta
155
What is an overriding aorta?
Entrance to the aorta is centered at the VSD instead of the main part of the left ventricle
156
What causes the right ventricular hypertrophy in tetralogy of fallot?
Pressure overload induced by pulmonary stenosis
157
What dictates the clinical severity of Tetralogy of Fallot?
Degree of pulmonary stenosis
158
What is the most common cyanotic congenital heart disease?
Tetralogy of Fallot
159
What murmur is heard with tetralogy of fallot?
Holosystolic murmur and/or systolic ejection murmur
160
What does the holosystolic murmur depend on in tetralogy of fallot?
Degree of VSD
161
What does the systolic ejection murmur depend on in tetralogy of fallot?
Degree of pulmonary stenosis
162
Infants with what in tetralogy of fallot require immediate intervention?
Severe pulmonary stenosis
163
Is right ventricular outflow tract or pulmonic valve stenosis progressive in tetralogy of fallot?
Yes
164
What are "tet" spells
Significant obstruction of the pulmonary outflow tract triggered by increased demand such as during period of excitement, crying, feeding, or increased activity
165
What are the symptoms of "tet" spells?
Cyanosis | Syncope
166
Why do children squat during "tet" spells?
Increases peripheral vascular resistance which decreases the degree of right to left shunting (allows them to oxygenate better)
167
Does clubbing of the fingers occur with tetralogy of fallot?
Yes
168
What is seen on x-ray in a patient with tetralogy of fallot?
Boot shaped heart
169
What causes the boot shaped heart seen with tetralogy of fallot?
Upturned cardiac apex caused by right ventricular hypertrophy and a concave pulmonary arterial segment
170
What happens in the classic form of transposition of the great arteries?
Right ventricle is connected to the aorta | Left ventricle is connected to the pulmonary trunk
171
Is transposition of the great arteries compatible with life?
No
172
What is often kept open if a baby is born with transposition of the great arteries?
Ductus arteriosus with prostaglandin E1
173
Transposition of the great vessels results in what type of shunt?
Right-to-left
174
Which ventricle hypertrophies in the transposition of the great arteries?
Right ventricle
175
What are the symptoms associated with transposition of the great vessels?
Cyanosis | Trouble breathing
176
What is tricuspid atresia?
Absence of the tricuspid valve
177
Is tricuspid atresia compatible with life?
No (not without ASD or VSD)
178
What is the left ventricle responsible for in transposition of the great vessels?
Pumping blood to both the right ventricle, lungs, and systemic circulation
179
What is needed immediately after birth for tricuspid atresia?
Surgical correction
180
What is coarctation of the aorta?
Obstructive defect which manifests as focal narrowing of the aorta
181
Which gender is coarctation of the aorta most common in?
Males
182
If females are seen with coarctation of the aorta what syndrome should be suspected?
Turner's syndrome
183
What is associated with half of the cases of coarctation of the aorta?
Bicuspid aortic valve
184
Patients with coarctation of the aorta have an increased risk of what?
Berry aneurysm which predisposes them to intracerebral hemorrhage
185
Infantile coarctation of the aorta is characterized by what?
Preductal coarctation (located before the ductus arteriosus) -> significantly less blood flow to the lower half of the body
186
Adult coarctation of the aorta is characterized by what?
Coarctation at the ductal arteriosus or in a postductal location
187
Diminished pulses is seen in which form of coarctation of the aorta?
Adult
188
Is there cyanosis with coarctation of the aorta?
Yes
189
What is seen on CXR with adult coarctation of the aorta?
Tortuous collateral intercostal vessels which cause pressure erosion of the inferior rib margins causing rib notching
190
What is the difference between the infantile and adult form of coarctation of the aorta?
Infantile form has a PDA | Adult for does NOT have a PDA
191
What does the clinical presentation of coarctation of the aorta depend on?
Severity of stenosis
192
What are the symptoms of the infantile form of coarctation of the aorta?
``` Cyanosis in lower extremities Absent lower extremity pulses Heart failure Shock Pale, irritable, diaphoretic, SOB ```
193
What are the symptoms of coarctation of the aorta without PDA?
``` Hypertension in upper extremities Hypotension in lower extremities Cold lower extremities Femoral artery pulse delay Pain in extremities with exercise ```
194
What hypertrophy is seen with coarctation of the aorta?
Concentric left ventricular hypertrophy (also heart failure)
195
Which valve dysfunctions can be see with aortic stenosis?
Hypoplastic (small) Dysplastic (nodular thickened) Abnormal cusp number
196
What hypertrophy is seen with aortic stenosis?
Concentric left ventricular hypertrophy (due to pressure overload)
197
What is hypoplastic left heart syndrome?
Aorta is stenotic or atretic and oxygenated blood flow is only possible through an atrial septal defect with a PDA
198
What is the blood flow in hypoplastic left heart syndrome?
Right ventricle -> lungs -> left atrium -> right heart (through ASD) -> right ventricle pumps blood to systemic (through PDA)
199
What hypertrophy is seen with pulmonary stenosis?
Right ventricular hypertrophy
200
What two complexes is pulmonary stenosis associated with?
Tetralogy of Fallot | Transposition of the Great Arteries
201
What are the causes of ischemic heart disease?
Atherosclerosis Coronary artery emboli Myocardial vessel inflammation (vasculitis) Vessel spasm
202
What are the classic clinical features of myocardial infarction?
``` Prolonged (>30 minutes) Substernal chest pain "Crushing, stabbing, squeezing" Radiate to neck, shoulder or jaw Rapid, weak pulse Profuse sweating Nausea, vomiting Dyspnea and discomfort ```
203
Nausea and vomiting are related to what specific MI location?
Posterior-inferior (due to vagal stimulation)
204
Diabetic neuropathy may hide symptoms of what?
Myocardial infarction
205
How is myocardial infarction diagnosed?
``` Symptoms EKG changes Cardiac markers (troponin) ```
206
Myocardial ischemia leads to loss of function after how many minutes?
1-2 minutes
207
Necrosis occurs how long after myocardial infarction?
20-40 minutes
208
How long after a MI is neurologic recovery unlikely?
5-7 minutes
209
How long after a MI is severe irreversible brain damage probable?
10 minutes
210
What is cardioplegia?
Heart is cooled significantly lowering the myocytes metabolic rate and preventing ischemic death
211
Oxygen consumption of myocytes drops 50% for every how much reduction in temperature?
10 degrees celsius
212
After MI how long before onset fo ATP depletion?
Seconds
213
After MI how long before loss of contractility?
Less than 2 minutes
214
After MI how long before ATP reduced to 50% of normal?
10 minutes
215
After MI how long before ATP is reduced to 10% of normal?
40 minutes
216
After MI how long before irreversible cell injury?
20-40 minutes
217
After MI how long before microvascular injury?
1 hour
218
What are the most specific and sensitive markers we have for acute myocardial infarction?
Troponin T | Troponin I
219
What are the function of troponin T and I?
Regulate calcium mediated contraction of cardiac muscle
220
Which troponin is currently used by most labs?
Troponin I
221
Which creatine kinase isoform is present in cardiac muscle?
MB heterodimer
222
Which creatine kinase isoform is present in muscle?
MM
223
What creatine kinase isoform is present in the brain and lung?
BB
224
Is CK-MB sensitive?
Yes
225
Is CK-MB specific?
No
226
What is released by cardiac muscle with injury but is nonspecific?
Myoblobin
227
Are troponin I and T normally detected in circulation?
No
228
What releases troponin I and T
Dead and dying cardiomyocytes
229
When does dying cardiomyocytes start releasing troponin?
3 hours
230
Why are serial troponin draws necessary?
Patient could have a heart attack prior to an increase in troponin levels
231
When does CK-MB go back to baseline?
48-72 hours after infarction
232
How long is troponin elevated for?
5 days
233
CK-MB is specifically utilized to assess for what?
Reinfarction of the heart after initial heart attack
234
When does CK-MB and troponin I peak?
24 hours
235
What arteries are most commonly occluded in MI?
LAD > right coronary artery > left circumflex artery
236
Occlusion of the LAD causes infarction of what?
Apex LV anterior wall Posterior 2/3 of septum
237
Occlusion of the left circumflex artery causes infarction of what?
LV lateral wall
238
Occlusion of the right coronary artery causes infarction of what?
RV free wall LV posterior wall Posterior 1/2 of septum
239
When does a subendothelial infarct occur?
``` Reperfusion of transmural infarct (regional) Global hypotension (circumferential) ```
240
What happens with a reperfusion of transmural infarct?
Blocking thrombus is dislodge either spontaneously or through thrombolytic therapy -> regional subendocardial infarct
241
When does global hypotension occur?
Shock/significant coronary artery stenosis -> circumferential subendocardial infarct
242
What is a multifocal microinfarction?
Numerous small infarcts occur within the smaller intramural vessels of the myocardium
243
What causes a multifocal microinfarction?
Cocaine use | Embolic disease
244
How do coronary artery perfuse the heart muscle?
Epicardium -> endocardium
245
What is the last portion of the heart to get perfused?
Myocardium near the endocardial surface
246
How do infarctions spread?
Inside of the heart out (necrotic core expands into the overlying tissue)
247
What perfuses the endocardium?
Blood in the heart chamber (this portion of the heart still viable despite the infarction)
248
What does the rate of necrosis throughout the heart depend on with a MI?
Degrees of collateral circulation with areas being fed by a single vessel taking a shorter time to become a transmural infarct
249
What is seen on the electron microscope at 0 hours?
Relaxation of myofibrils Glycogen loss Mitochondrial swelling
250
What is seen on light microscope from 0.5-4 hours?
Waviness of fibers at border (due to sarcolemmal disruption)
251
What is seen on electron microscope from 0.5-4 hours?
Sarcolemmal disruption | Mitochondrial amorphous densities
252
What is seen grossly from 4-12 hours
Dark mottling
253
What is seen on light microscope from 4-12 hours?
Early coagulation necrosis Edema Hemorrhage
254
What is seen grossly from 12-24 hours?
Dark mottling
255
What is seen on light microscope from 12-24 hours
``` Ongoing coagulative necrosis Pyknosis of nuclei Myocyte hypereosinophila Marginal contraction band necrosis Early neurtrophilic infiltrate ```
256
What is pyknosis?
Condensation of the chromatin in the nucleus
257
What is seen grossly from 1-3 days?
Mottling with yellow-tan infarct center
258
What is seen on light microscope from 1-3 days?
Coagulation necrosis Loss of nuclei and striations Brisk interstital infiltrate of neutrophils
259
What is seen grossly from 3-7 days?
Hyperemic border | Central yellow-tan softening
260
What is seen on light microscope from 3-7 days?
Beginning disintegration of dead myofibers with dying neutrophils Early phagocytosis of dead cells by macrophages at infarct border
261
What is seen grossly from 7-10 days?
Maximally yellow tan, and soft, with depressed red-tan margins
262
What is seen on light microscope from 7-10 days?
Well-developed phagocytosis of dead cells | Granulation tissue at margins
263
What is seen grossly from 10-14 days?
Red-gray depressed infarct borders
264
What is seen on light microscope from 10-14 days?
Well-established granulation tissue with new blood vessels and collagen deposition
265
What is seen grossly from 2-8 weeks?
Gray-white scar, progressive from border towards core of infarct
266
What is seen on light microscope from 2-8 weeks?
Increased collagen deposition | Decreased cellularity
267
What is seen grossly from 2 months?
Scarring complete
268
What is seen on light microscope from 2 months?
Dense collagenous scar
269
What is the first sign of irreversible injury in myocardial infarction?
Wavy fiber change
270
What causes the wavy fiber change after MI?
Mechanical pulling by viable fibers on dead fibers resulting in folding and twisting
271
What leaks out of dead myoctyes after 2-3 hours
Lactate dehydrogenase
272
What stain is used to identify lactate dehydrogenase after MI?
Triphenyltetrazolium chloride
273
Do areas of infarction hemorrhage or scar turn bright red with the triphenyltetrazolium choloride?
No
274
What happens cellularly with irreversible injury to myocytes?
Cell membrane disrupted with reperfusion Influx of calcium causing sarcomeres to contract Contraction bands on light microscopy (contraction band necrosis)
275
What replaces normal myocytes after MI?
Fibroblasts with increased collagen
276
What are early complications of MI?
``` Life threatening arrhythmia (v tach, v fib) Contractile dysfunction (shock) ```
277
What are intermediate complications of MI?
Rupture: septal, wall, papillary | Acute pericarditis
278
What are the late complications of MI?
``` Chronic pericarditis (Dressler syndrome) Ventricular aneurysm (remodeling) Continued risk of heart failure, life threatening arrhythmia ```
279
What causes mitral regurgitation after MI?
Ischemic papillary muscles
280
What is the most common mechanical complication of MI?
Papillary muscle rupture
281
Which infarct causes papillary muscle rupture?
Right circumflex artery
282
Which infarct causes ventricular septal rupture?
Anterior infarcts
283
What is the most common cause of death due to MI?
Fatal arrhythmias (v fib)
284
What is the second most common cause of death after MI?
Cardiogenic shock (pump failure due to contractile dysfunction due to the death of heart muscle)
285
When does myocaridal rupture typically occur after MI?
2-4 days
286
Myocardial rupture after MI requires what?
Transmural infarct
287
Rupture of the free wall can lead to what?
Blood accumulating in the pericardial space
288
What is blood accumulating in the pericardial space called?
Acute pericardial tamponade
289
What happens to the heart during acute pericardial tamponade?
Heart is unable to adequately fill during diastole because of the pressure of the blood in the pericardial sac
290
Septal rupture can lead to what?
VSD with left to right shunting
291
Papillary muscle rupture can lead to what?
Valve incompetence | Post infarct regurgitation
292
Why does myocardial rupture occur more often in the elderly?
Lower muscle mass
293
What is pericarditis?
Inflammation of the pericardium
294
What is present with acute pericarditis?
Pericardial friction rub
295
When does myocardial rupture and acute pericarditis occur post MI?
2-4 days
296
What are the risk factors for myocardial rupture?
Increased age First MI Absence of LV hypertrophy
297
Acute pericardial tamponade leads to what?
Hemodynamic collapse
298
When do late complications of MI occur?
After 2 weeks
299
What is Dressler syndrome?
Fibrinous pericarditis
300
What causes Dressler syndrome?
Immune response against myocardial proteins which are encountered by the immune system in the blood after a previous infarct Anti-heart antibodies which create an inflammatory reaction involving the pericardium
301
What is the end result of Dressler syndrome?
Febrile pericarditis Pericardial effusion Pleuritic pain
302
What causes the late complication of ventricular aneurysm post MI?
Thin scarred ventricular wall
303
What causes progressive heart failure after MI?
Inadequate compensatory response
304
What is seen grossly with Dressler syndrome?
Dark, roughened epicardial surface
305
What is the definition of angina pectoris?
Transient, often recurrent chest pain induced by myocardial ischemia insufficient to induce myocardial infarction
306
What are the three types of angina pectoris?
1) Stable angina 2) Prinzmetal variant angina 3) Unstable angina
307
What is released due to lack of oxygen in the heart muscle?
Adenosine | Bradykinin
308
Which patients often have silent angina?
Elderly Previous MI Diabetic neuropathy
309
What is stable angina?
Demand type of ischemia in that with increased physical activity or stress the heart becomes ischemic but when the patient is at rest there is an adequate supply of oxygen
310
What causes stable angina?
Stenotic occlusion of coronary artery
311
What are the symptoms of stable angina?
Substernal pressure, squeezing, burning
312
What relieves stable angina?
Rest | Vasodilators
313
What induces stable angina?
Physical activity | Stress
314
What is prinzmetal variant angina?
Episodic coronary artery spasm
315
What makes prinzmetal variant angina worse?
Aterosclerotic disease
316
When does prinzmetal variant angina occur?
At rest
317
Is prinzmetal variant angina associated with physical activity?
No
318
What is the pattern of prinzmetal variant angina?
3-6 month clusters of recurrent attacks separated by asymptomatic periods
319
What is given to to alleviate the symptoms of prinzmetal variant angina?
Vasodilators (nitrate)
320
What is unstable angina?
Angina which is present at rest or angina that increases in frequency or duration
321
What is the most common cause of unstable angina with acute chest pain with activity and rest?
Rupture of atherosclerotic plaque which results in a non-occlusive thrombus
322
What causes unstable progresive angina?
Progressive obstruction
323
What type of pattern is there with unstable angina?
Crescendo patern
324
When is table angina symptomatic?
Only with increased demand for oxygen during exercise or activity
325
Unstable angina is due to what?
Problem with overall supply of oxygen even at rest
326
ST elevation on EKG corresponds with what?
Transmural infarction
327
When there isn't a ST elevation on EKG what is on the differential?
NSTEMI | Unstable angina
328
What can be used to tell the difference between NSTEMI and unstable angina?
Presence of troponin
329
Is troponin elevated in NSTEMI?
Yes
330
Is troponin elevated in unstable angina?
No
331
Does unstable angina or NSTEMI show ST elevations?
No

CPR 2 Exam 1 (20 decks)

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