Flashcards in Cardiovascular: Pathoma, BRS, First Aid Deck (318):
1
Ischemic heart disease is caused by what?
Partial or complete interruption of arterial blood flow to the myocardium
2
What is the main cause for interruption of arterial blood flow to myocardium?
Atherosclerosis of coronary arteries
3
Incidence of IHD increases with what?
Age
4
How will ischemia present? (6)
1. Silent
2. Angina pectoris
3. Coronary steal syndrome
4. Myocardial infarction
5. Sudden cardiac death
6. Chronic ischemic heart disease
5
Frequency of IHD increases in patients who manifest what?
Metabolic syndrome
6
What does metabolic syndrome include?
1. Central obesity
2. Artherogenic lipid patterns
3. Hypertension
4. Insulin resistance
5. Proinflammatory state
7
What predisposes someone to metabolic syndrome?
Obesity
Physical activity
Genetic factors
8
What is angina pectoris?
Episodic chest pain that is caused by inadequate oxygenation of myocardium
9
How much stenosis or obstruction of a vessel is needed to cause angina?
>70-75%
10
Is there myocyte necrosis in angina?
Why?
No
Reversible
11
What is the most common type of angina?
Stable angina
12
What precipitates stable angina?
Why?
Exertion or stress
Can't get enough blood (oxygen) to heart
13
What causes stable angina?
CAD of coronary arteries greater than 70%
14
How does stable angina present? 3
1. Chest pain less than 20 minutes that radiates to left arm or jaw
2. Diaphoresis
3. Shortness of breath
15
Why is the 20 minute interval important?
After that you get irreversible injury and cell death
16
What does an EKG show in stable angina?
Why?
ST segment depression
Subendocardial ischemia
17
What relieves stable angina? (2)
1. Rest
2. Vasodilators like nitroglycerin
18
Function of nitroglycerin?
Vasodilation of veins mainly that decreases preload and decreases stress on myocardia
19
Unstable angina is chest pain that occurs when?
At rest
20
What causes unstable angina?
Rupture of atherosclerotic plaque with thrombosis and incomplete occlusion of coronary artery
21
What type of damage is occurring in unstable angina?
Reversible injury to myocytes
22
What does an EKG show on unstable angina?
ST segment depression
23
What relieves unstable angina?
Nitroglycerin: Vasodilation to decrease preload which decreases stress
24
What are unstable angina patients at risk for?
Progressing to full occlusion: Myocardial infarction)
25
Prinzmetal angina is due to what?
Coronary artery vasospasm
26
What is the timing of pain in prinzmetal angina?
Episodic/intermittent chest pain at rest
27
What type of damage occurs in prinzmetal angina?
Reversible injury to myocytes
28
What does prinzmetal EKG show?
Why
ST segment elevation
Transmural ischemia
29
What relieves prinzmetal angina? 2
1. Nitroglycerin: Decrease preload
2. Calcium channel blockers: Decrease spasm
30
What is the most important cause of morbidity from IHD?
Myocardial infarction
31
What is myocardial infarction?
Necrosis of cardiac myocytes (so after 20 minutes)
32
What mainly causes a myocardial infarction?
Rupture of a atherosclerotic plaque with thrombosis and complete occlusion of coronary artery
33
Other causes of myocardial infarction? (3)
1. Coronary artery vasospasm (Complete prinzmetal)
2. Emboli
3. Vasculitis (kawasaki's disease)
34
Symptoms of myocardial infarction?
1. Severe chest pain greater than 20 minutes that radiates to left arm/jaw
2. Diaphoresis
3. Dyspnea: Heart can't pump --> Fluid in lungs
35
Will nitroglycerin relieve myocardial infarction pain?
No
36
What ventricle is usually involved in an MI?
Left
37
What is most common artery involved in MI?
Which causes an infarction where?
LAD
Infarciton of anterior wall of LV and anterior part of IV septum
38
What is 2nd most common artery involved in MI?
Which causes an infarction where?
Right coronary
Infarction of right ventricle, posterior wall of LV and anterior portion of IV septum
39
What is 3rd most common artery involved in MI?
Which causes an infarction where?
Left circumflex
Infarction of lateral wall of LV
40
What are the 2 types of infarction based on heart layers involved?
Which is more common
1. Transmural: Entire ventricular wall from endo to epi. More common
2. Subendocardial infarction: Just 1/3 of the wall
41
ECG shows what during myocardial infarction?
1. During the initial subendocardial infarction, ST depression
2. During later transmural infarction, ST elevation
42
Why are there biomarkers for MI?
Irreversible damage to myocytes causes membrane breakdown thus releasing markers
43
What is the most SENSITIVE and most SPECIFIC cardiac marker?
Troponin I
44
When does troponin I peak?
24 hours
45
How long does troponin I remain high after MI?
7 to 10 days
46
CK-MB is most useful for what?
Detecting re-infarction
47
When does CK-MB rise?
4-6 hours after infarction
48
When does CK-MB peak?
24 hours
49
When does CK-MB return to normal? 72 hours
72 hours
50
What is the gold standard for diagnosing MI in first 6 hours?
ECG
51
When does LDH peak?
How long does it last?
3 days
4-7 days
52
When does myoglobin peak?
How long does it last?
First 6 hours
24 hours
53
Treatment of MI includes what? 6
Describe each
1. ASA/Heparin: limit more thrombosis
2. Supplemental O2: minimize ischemia
3. Nitrates: Vasodilate --> Decrease preload
4. Beta-blocker: Slow heart rate --> Decrease O2 need + decrease arrhythmia
5. ACE inhibitor: Decrease dilatation
6. Fibrinolysis/Angioplasty: Destroy blockage/open up vessel
54
How does an ACE inhiabitor decrease LV dilatation? 2
1. Blocks ANG II production --> prohibit constriction of peripheral arterioles --> Decrease afterload
2. Block ANG II --> No aldosterone secreted --> No blood volume increase
55
Two injuries due to fibrinolysis and angioplasty?
1. Contraction band necrosis
2. Reperfusion
56
What is contraction band necrosis?
Calcium will enter cell after blood flow is restored and cause contraction --> visible contraction bands
57
What is reperfusion injury?
Returning O2 rapidly to cell causes ROS to form --> Further damage the cells
58
What is a lab test for reperfusion injury?
See cardiac enzymes continue to rise after reperfusion
59
Less than 4 hours from infarction, what risks does patient have?
1. Cardiogenic shock: Heart fails --> Hypofusion
2. CHF: Dead tissue --> Can't pump--> Backs up into heart --> Decreased ejection fracture
3. Arrhythmia
60
Between 4 and 24 hours after infarction, what changes do you see macroscopically?
What risk?
1. Dark discoloration
2. Coagulative necrosis: Karyolysis, pyknosis, karyorrhexis
Arrhythmia
61
Between 1 and 3 days what change do you see? 2
What is patient at risk for?
Yellow pallor
Neutrophils on scene
Fibrinous pericarditis
62
How does fibrinous pericarditis present in days 1-3?
Why does it occur?
Chest pain with friction rub
Transmural infarction --> Neutrophils enlame entire wall --> Debris into pericardium --> Pericarditis
63
How does MI present in days 4-7? 2
1. Yellow pallor
2. Macrophages on scene
64
What is important about days 4-7 after MI?
Cardiac wall is weakest due to macrophages eating all the dead material.
65
What are the 3 things a patient is at risk for 4-7 days after MI?
1. Rupture of ventricular free wall --> Blood leaks into pericardium --> Compresses heart --> Cardiac tamponade
2. Rupture of IV septum --> Shunt from LV to RV
3. Rupture of papillary muscle --> Mitral insufficiency
66
What causes rupture of papillary muscle?
Occlusion of right coronary artery
67
In weeks 1-3, what are the macroscopic changes? (2)
1. Red border as granulation tissue enters from edge
2. Granulation tissue with fibroblasts, collagen, and BV's
68
Months after, what changes does MI patient have?
1. White scar of Type 1 collagen
2. Fibrosis
69
What risks does a patient with an MI have after months? (3)
1. Weak scar: leads to balloon like dilatation --> Aneurysm
2. Scar along heart wall --> Stasis --> Mural thrombus
3. Dressler syndrome
70
What happens in Dressler's syndrome?
Transmural infarct --> Pericardium leaks --> Form imune response against pericardium antigens --> Pericarditis 6-8 weeks after infarction
71
What is most common cause of death in first several hours after infarction?
Arrhythmia
72
What is sudden cardiac death due to?
Cardiac disease
73
How does sudden cardiac death appear? 2
1. Asymptomatic before
2. Less than 1 hour after symptoms arise
74
What usually causes sudden cardiac death?
Fatal ventricular arrhythmia
75
Most common etiology of sudden cardiac death?
Acute ischemia
76
90% of SCD patients have what pre-existing condition?
Severe atherosclerosis
77
Less common etiologies of SCD? 3
1. Mitral valve prolapse
2. Cardiomyopathy
3. Cocaine abuse
78
Chronic ischemic heart disease is defined how?
Poor myocardial function
79
What is Chronic IHD due to?
Chronic ischemic damage (with or without MI)
80
What do chronic IHD patients progress to?
CHF
81
What is coronary steal syndrome?
Vasodilator may aggravate ischemia by shunting blood from area of critical stenosis to an area of higher perfusion.
82
Congestive heart failure may be failure of what ventricle?
Right, Left or both
83
Causes of Left sided heart failure?
Explain each
1. Ischemia: Decrease blood flow --> Damage myocardium --> Can't pump well
2. Hypertension: Get concentric LV hypertrophy to deal with stress --> Extra O2 demands --> Ischemic damage --> Can't pump well
3. Dilated cardiomyopathy: Stretch all four chambers --> Can't contract well
4. Myocardial infarction: Nonfunctional tissue --> Can't pump well
5. Restrictive cardiomyopathy: Can't fill heart well --> Can't pump enough out
6. Aortic and mitral valvular disease
84
Two main Clinical manifestations of LCHF?
1. Pulmonary congestion
2. Decreased forward perfusion
85
Pulmonary congestion from LCHF is due to what?
Heart can't pump blood forward --> Backs up -->blood accumulates in lung --> Pulmonary congestion
86
Why does pulmonary congestion result in dyspnea?
Increase in hydrostatic pressure --> Pulmonary edema --> Dyspnea
87
What is PND?
Dyspnea upon laying flat for several hours
88
What is othopnea?
Dyspnea if late flat for a few minutes?
89
What are crackles?
Fluid in lungs upon auscultation
90
Ruptured pulmonary capillaries in LCHF results in what?
Blood in alveoli --> Macrophages arrive to clean up --> Iron fills maccrophages --> Forms hemosiderin laden cells called heart failure cells.
91
What are the 5 clinical manifestations of pulmonary congestion?
1. Dyspnea
2. PND
3. Orthopnea
4. Crackles
5. Heart failure cells
92
Decreased forward perfusion results in activation of what?
RAS
93
RAS activation has what two effects?
Decreased blood flow to kidneys activates juxtaglomerular apparatus --> Release renin --> Release Ang II -->
1. Constrict arterioles --> Increase total peripheral resistance
2. Go to adrenal gland --> Release aldosterone --> Cause resorption of sodium --> Water follows --> Increase blood volume
OVERALL = Increase resistance --> Exacerbates problem
94
Main treatment for LCHF?
ACE inhibitor
95
Right sided failure has what causes? 6
1. Left sided heart failure
2. Left-sided lesions
3. Pulmonary hypertension: Chronic lung disease/cor pulmonale --> Vessel constriction
4. Cardiomyopathy/Diffuse myocarditis
5. Tricuspid or pulmonary valvular disease
6. Left to right shunts
96
Most common cause of RCHF?
Why?
LCHF
Backup into pulmonary circuit --> Backups into right heart
97
Isolated RCHF is usually due to what?
Cor pulmonale
98
Clinical manifestations of RCHF? 4
1. Jugular vein backup --> JVD
2. Hepato and spleno congestion --> Hepatosplenomegaly + cardiac cirrhosis + nutmeg liver
3. Pitting edema: Due to increased hydrostatic pressure in low extremities.
4. Renal hypoxia: Fluid retention
99
Congenital defects arise when?
During embryogenesis weeks 3-8
100
Congenital heart defects are seen in what percentage of live births?
1%
101
Most congenital defects are caused by what?
Undetermined = Sporadic
102
Congenital defects overall usually result in what?
Shunting between left and right circulations
103
What is most common congenital heart defect?
Ventricular septal defect
104
VSD is a defect associated with what syndrome?
Fetal Alcohol Syndrome
105
What happens with blood flow in VSD?
Blood enters right atrium and can enters normal low pressure RV over high pressure LV. However upon returning to LA, blood chooses low pressure RV instead of high pressure LV resulting in LEFT TO RIGHT SHUNT
106
How does size of defect affect symptoms in VSD?
Small VSD = asymptomatic
Large VSD = large amounts of blood entering RV --> increase of blood in pulmonary circuit --> Pulmonary hypertension
107
What does pulmonary hypertension from VSD result in over time?
P-HTN --> Right side to become high pressure --> Blood now shunts from high pressure right to low pressure left ventricle --> Deoxygenated blood in systemic circulation --> Cyanosis
108
The reversal of a shunt due to a change in pressure from pulmonary hypertension is known as what?
Eisenmenger syndrome
109
3 consequences of Eisenmenger's syndrome?
1. RV hypertrophy: Due to pumping against higher pressure
2. Polycythemia: Deox blood --> Hypoxemia --> Release EPO --> Increase RBC's
3. Clubbing: Change in fingernails from cyanosis
110
Treatment of VSD? (2)
1. Small VSD close on their own
2. Surgical closure
111
Atrial septal defect includes what five types?
1. Patent foramen ovale
2. Septum primum
3. Septum secundum
4. Sinus venosus
5. Lutembacher syndrome
112
Patent foramen ovale is clinically significant how?
It's not. 20-30% of people have it.
113
Septum primum/Ostium primum is associated with what consequence?
What genetic disease is associated with this?
Affects lower part of septum so it can affect AV valves.
Down's syndrome
114
Most common type of ASD is what?
Ostium/Primum secundum
115
Ostium/Primum secundum is a defect in what?
Fossa ovalis
116
Sinus venosus affects what area?
Upper part of septum near SVC
117
Lutembacher syndrome has what two components?
1. ASD
2. Mitral stenosis
118
Atrial septal defect results in what type of shunt?
Left to right shunt
119
ASD presents how on auscultation? 2
1. Split S2
2. Loud S1
120
Why does split S2 occur in ASD?
Blood from high pressure LA crosses to low pressure RA --> Extra volume on right side --> Delayed closure of pulmonic valve --> Split S2
121
What is the S2 sound?
Pulmonary and aortic valves closing
122
What is an important complication of ASD?
Paradoxical emboli: DVT emboli enters RA normally but crosses over to LA and lodges in brian or extremities.
123
When are ASD symptoms seen?
What is the main one?
Late in life
Cyanosis due to Eisenmenger's syndrome from P-HTN
124
What is Patent ductus arteriosus?
Failure of ductus arteriosus to close.
125
PDA is associated with what situations? 2
1. Congenital Rubella
2. People living in high altitudes
126
What is the mechanism of PDA?
Blood enters RA --> RV --> Enters pulmonary artery --> Chooses to enter low pressure lungs over high pressure aorta --> LA --> Enters LV --> Enters aorta --> Chooses low pressure lungs over high pressure systemic circulation --> LEFT TO RIGHT SHUNT
127
What happens over time in PDA patients?
P-HTN develops --> Blood now chooses low pressure aorta over high pressure lungs --> Deox blood goes to LOWER extremities --> Cyanosis in lower extremities in late life.
128
How does PDA appear at birth?
Asymptomatic left to right shunt
129
What causes PDA to appear in adulthood?
Eisenmenger's syndrome
130
What keeps the PDA open? 2
Prostaglandin E
Low O2 tension
131
What are treatments for PDA? (2)
1. surgery
2. Indomethacin
132
Function of indomethacin
Decrease prostaglandin E --> Close PDA
133
What is the quality of murmur in PDA?
Machine-like murmur
134
Tetralogy of Fallot is caused by what?
Anteriosuperior displacement of infundibular septum
135
Tetralogy of Fallot has what four components?
PROVe
Pulmonary infundibular stenosis
Right Ventricular Hypertrophy
Overriding aorta (of VSD)
Ventricular Septal Defect
136
What is the flow of blood in tetralogy of Fallot?
RA --> RV --> Due to stenosis --> Shunt to aorta = Right to left shunt
137
In babies, ToF results in what?
Cyanosis due to deoxygenated right sided blood entering systemic circulation.
138
What is shape of heart in ToF?
Boot-shaped heart
139
In adults, what will cause cyanosis to occur in ToF?
Exercise
140
How do patients deal with ToF?
Squat --> Increase left sided pressure --> Decrease shunt --> Oxygenate more blood --> less cyanotic
141
The main point behind squatting with ToF?
Increased arterial resistance --> Decreases shunting
142
Treatment of ToF?
Early surgery
143
In transposition of great vessels, what happens?
Aorta comes off RV and Pulmonary artery comes off LV resulting in two independent circuits that do not connect.
144
Can a person with transposition of great vessels live?
Only if they somehow form a shunt.
145
How do you treat Transposition of great vessels?
Specifically? (2)
Cause open PDA so that blood can mix
1. Give patient prostaglandin E
2. Surgically repair problem
146
What maternal condition is associated with Transposition of Great vessels?
maternal diabetes
147
How do ToGV patients present?
Early cyanosis since deox blood from right side enters aorta --> Systemic circulation
148
What is truncus arteriosus?
Truncus fails to divide providing one single large vessel coming from both ventricles.
149
How does blood flow in truncus arteriosus?
One vessels drains both ventricles but divides later --> Deox and ox blood mix --> Deox blood enters systemic circulation --> Cyanosis
150
What is tricuspid atresia?
Tricuspid valve orifice fails to develop
151
What does atresia mean?
Fail to form lumen of tube
152
In tricuspid atresia, how is the RV described?
Hypoplastic
153
In tricuspid atresia, what is the situation associated with?
What is flow of blood?
How does it present?
ASD: Right to left shunt
Tricuspid fails to form --> No blood to RV --> ASD forms --> Deox blood enters left side
Cyanosis
154
Coarctation means what?
Narrowing of aorta
155
Coarctation of aorta is divided into what two forms?
Infantile and Adult
156
Infantile CoA is associated with what?
PDA
157
In infantile CoA, where is the coarctation?
Distal to aortic arch
Proximal to PDA
158
Describe the pressures in infantile CoA?
High pressure above coarctation
Low pressure below coarctation
159
What is mechanism of blood flow in infantile CoA?
RA--> RV --> PA --> Cross PDA to low pressure aorta below coarctation --> Deox blood in lower extremities --> Lower extremity cyanosis
160
What disease is associated with infantile CoA?
Turner's
161
Is adult form of CoA associated with PDA?
NO
162
Where is coarctation in adult CoA?
Distal to aortic arch?
163
Mechanism of blood flow in adult CoA?
Since narrowing is below arch --> High pressure above and low pressure below --> High pressure in UE + low pressure in LE
164
How does adult CoA present?
HTN in upper extremity
Hyptension with weak pulses in lower extremity
165
When is adult form of CoA found?
In adulthood
166
What defect is adult CoA associated with?
Bicuspid aortic valve
167
What X-ray feature is seen in adult CoA?
Why?
Notching of ribs
Collateral circulation develops across intercostal arteries --> Engorged arteries --> Notching of ribs
168
What is Turner's syndrome associated with in congenital heart defects?
Coarctation of Aorta (Infantile)
169
What are congenital defects are Down syndrome patients known for?
Such as? 3
Endocardial cushion defects
ASD, VSD, AV septal defect
170
Congenital rubella is associated with what congenital CV defects? 5
Septal defects: VSD,
PDA
Pulmonary artery stenosis
Valvular stenosis
Aortic stenosis
171
22q11 syndromes are associated with what CV defects? (2)
1. Truncus arteriosus
2. Tetralogy of Fallot
172
Marfan's syndrome is associated with what CV defects?
Aortic insufficiency and dissection
173
Infant of diabetic mother has what associated CV defects?
Transposition of great vessels
174
Noncyanotic congenital CV defects include what two types?
No shunt
Left-to-right shunt
175
What are the diseases of noncyanotic congenital CV defects?
No shunts = 1. Aortic stenosis 2. CoA
L-2-R shunts = 1. PDA, ASD, VSD
176
Rank frequency of left to right shunt defects?
VSD > ASD > PDA
177
Right to left shunts are known as what? 3
Blue babies
Early cyanosis
Cyanotic diseases
178
What are the 5 T's of right to left shunts?
Tetralogy of Fallot
Transposition of great arteries
Truncus arteriosus
Tricuspid Atresia
Total anomalous pulmonary venous return
179
What do most patients with truncus arteriosus also have?
VSD
180
What is total anomalous pulmonary venous return?
Pulmonary veins return to RA
181
Two types of valvular disease?
Stenosis and regurgitation
182
Acute rheumatic fever is what?
Systemic complication of pharyngitis due to Group A beta-hemolytic strep
183
How old are children usually with ARF?
How many weeks after strep throat is ARF seen?
5-15 years old
2-3 weeks
184
What is the etiology of ARF?
The Bacterial M protein of Group A strep resembles human tissues and causes type II hypersensitivity against own heart tissues.
185
What evidence prior to ARF must be had?
How is this accomplished? 2
Evidence of group A strep infection
ASO or anti-DNase B titer
186
Minor criteria for ARF? 2
Fever
Elevated ESR
187
Major criteria for ARF?
JONES
J = Joint problems = Migratory polyarthritis
O = Heart problems (pan-carditis)
N = Nodules in Skin
E = Erythema marginatum
S = Sydenham's chorea
188
What is first layer of heart to be affected in ARF?
Which results in what?
Endocardium
Tiny vegetations on mitral valve (possibly aortic as well) --> Regurgitation
189
Myocardium is second layer to be affected in ARF, what forms here?
Aschoff bodies of: Giant cells + Fibrinoid material (degenerated collagen) + Anitschkow Cells
190
How do anitschkow cells appear?
Slender wavy nuclei (Caterpillar nuclei)
191
Pericarditis in ARF presents how?
Friction rub
192
Which of the 3 layers of carditis is most likely to kill ARF patient?
Myocarditis
193
What is erythema marginatum?
Rash that is more red on edges
194
Sydenham's chorea is what?
Rapid involuntary muscle movement
195
What is the First Aid acronym for Rheumatic fever facts?
FEVERSS
F=Fever
E=Erythema Marginatum
V=Valvular damage (vegetation and fibrosis)
E=Elevated ESR
R = Red-hot joints (migratory polyarthritis)
S=Subcutaneous nodules
S=St. Vitus' dance (Sydenham's chorea)
196
Rheumatic endocarditis has what happen in early stage?
Valve leaflets are red and swollen with tiny vegetations resulting in mitral valve regurgitation
197
As a consequence of healing, what changes do valves have in ARF?
Valves become thickened, fibrotic and deformed.
198
Chronic rheumatic valvular disease is result of what?
Valve scarring that results from rheumatic fever?
199
Chronic rheumatic valvular disease results in what?
Stenosis
200
Mitral valve stenosis leads to what?
Thickening of chordae tendinae and cusps
201
Aortic valve in CRV results in what?
Fusion of comissures
202
Fusion of comisures in aortic valve CRV results in what? (2)
1. Small orifice --> FIshmouth appearance
2. Stenosis --> Can't completely open valve
203
Mitral stenosis causes what pressure difference to develop?
Diastolic pressure higher in left atrium than in left ventricle
204
What is aortic stenosis
Narrowing of aortic valve orifice
205
What is aortic stenosis due to mainly? (2)
1. Fibrosis
2. Calcification
206
When does aortic stenosis present?
Late adulthood (>60 years old)
207
Two others causes of aortic stenosis?
Bicuspid aortic valve
Chronic rheumatic valve disease
208
Aortic valve is usually what organization?
Tricuspid
209
What's the problem with bicuspid aortic valves?
Two cusps do the work of 3 --> increases risk for aortic stenosis
210
How does CRVD cause aortic stenosis?
It has mitral valve stenosis and fusion of aortic valve comissures
211
What is difference between "wear-and-tear" aortic stenosis and CRVD caused aortic stenosis
Wear and tear aortic stenosis has only the aortic valve affected, CRVD = mitral + aortic valve
212
Compensation in aortic stenosis leads to what? 2
1. longer asymptomatic stage
2. Systolic ejection click followed by crescendo-decrescendo murmur
213
Complications resulting from aortic stenosis? (3)
1. LV Hypertrophy: Due to pumping against stenotic valve
2. Angina and syncope with exercise: Stenosis reduces systemic blood flow --> Don't get enough during exercise
3. Microangiopathic hemolytic anemia: Blood cells rupture moving across bad valve
214
Treatment of aortic stenosis?
Replace valve after symptoms appear
215
Aortic regurgitation is what?
backflow of blood from aorta into LV during diastole
216
AR arises due to what? 4
Which is most common
1. Isolated aortic root dilation (Most common)
2. Syphilitic aneurysm
3. Valve damage (such as CRVD)
4. Non-dissecting aortic aneurysm
217
Why does aortic root dilatation cause AR?
Dilation of root --> Pulls valves apart --> Regurg occurs
218
Clinical features of AR? 7
BE-PHILE
1. Bounding pulses
2. Early blowing diastolic murmur
3. Pulsating nail bed
4. Head bobbing
5. Increasing pulse pressure
6. LV dilation
7. Eccentric hypertrophy of one part of ventricle
219
Treatment of AR?
Valve replacement
220
What is the most common valvular lesion?
Mitral valve prolapse
221
What is mitral valve prolapse?
Ballooning of mitral valve into left atrium during systole
222
Mitral valve prolapse is due to what?
Myxoid degeneration of valve making it floppy
223
What diseases commonly have mitral valve prolapse? 2
Marfan and Ehlers Danlos
224
Clinical features of MVP? 3
1. Mid-systolic click with systolic regurgitation murmur
2. Arrhythmia
3. Can turn into infective endocarditis
225
Treatment of MVP?
Valve replacement
226
Mitral regurg involves what?
Reflux of blood from LV into LA during systole
227
Mitral regurg is a complication of what prior problem usually?
Mitral valve prolapse
228
Other causes of mitral regurg? 4
1. LV dilation
2. Infective endocarditis (Bad leaflets)
3. ARF (Mitral valve)
4. Papillary muscle rupture after MI
229
Clinical features of mitral regurgitation? 3
1. Holosystolic blowing murmur
2. Louder with squatting and expiration
3. volume overload and left-sided heart failure
230
Why does squatting make mitral regurg louder?
Increase systemic resistance --> less blood forward --> more blood backwards --> Louder murmur
231
Why does expiration make mitral regurg louder?
Increase in amount of blood entering LA --> Increase blood in LV --> increase in regurgitated blood
232
What is mitral stenosis?
Narrowing of mitral valve orifice
233
Cause of mitral stenosis?
CRVD
234
Clinical symptoms of mitral valve stenosis?
1. Opening snap with diastolic rumble
2. Volume overload leads to dilation of LA
235
Consequences of dilated LA in mitral valve stenosis?
1. Pulmonary congestion: Overloading LA --> Blood backs up into pulmonary circuit --> Pulmonary congestion --> Edema + Alveolar hemorrhage --> Heart failure cells
2. Pulmonary HTN: Excess blood in circuit --> Rt heart pumps against --> Right heart fails
3. Atrial fibrillation: Dilation --> Abnormal wall movement --> Stasis --> Mural thrombi
236
What syndrome is tricuspid valve involved in?
Carcinoid syndrome
237
The pulmonary valve is normally affected by what
Congenital malformations
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Endocarditis is what?
Inflammation of endocardium (inner surface)
239
Endocarditis is usually the result of what?
Infection
240
General features of bacterial endocarditis? 3
1. Large soft vegetations on valvular surfaces
2. Ulceration and perforation of valves cusps
3. Rupture of chordae tendineae
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Two classifications of bacterial endocarditis?
Acute endocarditis
Subacute endocarditis
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What is acute endocarditis caused by?
Highly virulent pathogens like staph aureus
243
Staph aureus is most common cause of endocarditis in what demographic?
IV drug abusers
244
Acute endocarditis like staph aureus is secondary to what?
Infection elsewhere
245
What is state of valves that highly virulent bacteria like staph aureus inhabit?
Normal healthy
246
What does acute endocarditis result in?
Large vegetations with rapid onset of symptoms due to destruction of valve
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Subacute endocarditis is caused by what?
Less virulent bacteria like strep viridans
248
What is the most common cause of bacterial endocarditis?
Strep Viridans
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Subacute endocarditis occurs on what state of valves?
Previously damaged valves such as congenital heart disease or valvular heart disease
250
What is result of subacute endocarditis?
subendocardium is exposed allowing for formation of thrombotic vegetations that do not destroy the valve.
251
What allows for bacteria in subacute endocarditis to inhabit a valve?
Bacteremia such as during a dental procedure
252
Staph epidermidis is most common in what?
Endocarditis of prosthetic valves
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Strep bovis is seen in what patients?
Endocarditis of patients with underlying colorectal carcinoma
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Endocarditis with negative blood cultures is due to what?
HACEK organisms
Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
255
Clinical features of bacterial endocarditis? 8
FROM JANE
1. Fever
2. Roth's spots
3. Osler nodes: Painful lesions on fingers/toes
4. Murmur: Vegetations disrupt flow
5. Janeway Lesions: nonpainful on palms/soles
6. Anemia
7. Nailbed hemorrhage
8. Emboli (septic): Vegetations come off and lodge
256
What valve is most frequently involved in bacterial endocarditis?
Mitral valve
257
Tricuspid valve bacterial endocarditis is associated with what?
IV drug abuse (Don't Tri Drugs)
258
Lab features of bacterial endocarditis? 5
1. Positive blood cultures
2. Microcytic anemia: Low hemoglobin, low MCV
3. Hepcidin traps iron
4. Ferritin will be hidden (Low TIVC)
5. TEE = best for detecting lesions on valves
259
Nonbacterial thrombotic endocarditis is what?
Where do vegetations arise?
What do they cause?
Sterile vegetations that arise with hypercoagulable state or underlying adenocarcinoma
Mitral valve along lines of closure
Regurgitation
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Libman-Sacks endocarditis is what?
Sterile vegetations associated with SLE (lupus)
261
What makes the vegetations in Libman-Sacks endocarditis special?
What does it result in?
Vegetations present on surface AND undersurface of mitral valve
Results in mitral regurgitation
262
The cause of endocarditis of carcinoid syndrome is what?
Secretory products of carcinoid tumors (vasoactive peptides and amines)
263
What does endocarditis of carcinoid syndrome result in?
Thickened endocardial plaques
264
What is cardiomyopathy?
Disease of heart muscle that results in cardiac dysfunction
265
What is most common form of cardiomyopathy?
Dilated cardiomyopathy (90%)
266
Dilated cardiomyopathy involves dilation/stretching of what?
All four chambers of heart
267
What are causes of dilated cardiomyopathy? (6)
MIDCAP BC
1. Idiopathic (Most common)
2. mutation (AD)
3. Coxsackievirus
4. Alcohol abuse
5. Drugs: Doxorubicin, Cocaine
6. Pregnancy: late or right after birth
7. wet Beriberi
8. Chagas disease
268
Treatment of dilated cardiomyopathy?
Transplant
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Hypertrophic cardiomyopathy is what?
Massive hypertrophy of left ventricle
270
What causes hypertrophic cardiomyopathy?
Genetic mutations in sarcomere proteins (autosomal dominant)
271
Clinical features of hypertrophic cardiomyopathy? 3
1. Decreased cardiac output: Too much muscle --> Lose compliance --> Diastolic dysfunction
2. Sudden death due to ventricular arrhythmias
3. Syncope with exercise: IV septum creates block in LV --> Blood can't get out well
272
What genetic disease is associated with hypertrophic cardiomyopathy?
Friedreich's ataxia
273
Microscopic features of hypertrophic cardiomyopathy?
Disoriented, tangled, hypertrophied myocardial fibers
274
Treatment of hypertrophic cardiomyopathy?
1. Beta blocker
2. Calcium channel blocker
275
Restrictive cardiomyopathy is what?
Diastolic problem of not being able to fill due to decreased compliance of ventricular myocardium.
276
Causes of restrictive cardiomyopathy?
A SHELF
Amyloidosis
Sarcoidosis: Granulomas in wall of heart
Hemochromatosis: Iron in wall of heart
Endocardial fibroelastosis: FIbrosis in endocardium
Loeffler Syndrome: Eosinophil infiltrate of heart
Fibrosis Postradiation
277
Which cause of restrictive cardiomyopathy is seen in children?
Endocardial fibroelastosis
278
How does restrictive cardiomyopathy present? (3)
1. CHF: Can't fill heart --> Backs up
2. Low-voltage EKG
3. Diminished QRS amplitudes
279
Two cardiac tumor types?
1. Myxoma
2. Rhabdomyoma
280
Myxoma is what?
Mesenchymal proliferation with gelatinous appearance to tumor
281
Myxoma has abundant what?
Ground substance
282
Myxoma is most primary cardiac tumor in what demogrpahic?
Adults
283
Can myocytes form tumors?
No
284
How does myxoma present?
Pedunculated mass in left atrium obstructing the mitral valve --> Syncope
285
What is rhabdomyoma?
Hamartoma of cardiac muscle
286
Rhabdomyoma is most common primary cardiac tumor in what demographic?
Children
287
Rhabdomyoma is associated with what disease?
Tuberous sclerosis
288
Where does rhabdomyoma grow?
Ventricle
289
Are myxoma and rhabdomyoma benign or malignant?
Benign
290
What is the most common heart tumor?
A metastasis
291
Common metastases primary locations?
1. Breast carcinoma
2. Lung carcinoma
3. Melanoma
4. Lymphoma
292
Metastases usually invade what layer of heart?
Resulting in what?
Pericardium
Pericardial effusion
293
Myocarditis most often presents as what?
Biventricular heart failure in young people with no other major heart diseases
294
Myocarditis morphological characteristics? 2
1. Diffuse myocardial degeneration
2. Necrosis with inflammatory infiltrate
295
Myocarditis has what etiology?
Specifically?
Viral
Coxsackievirus
296
What causes myocarditis in south america?
Chagas disease
297
What is hydropericardium?
Accumulation of serous transudate in pericardial space
298
What causes hydropericardium?
Most often?
Anything that can cause systemic edema.
Hypoproteinemia like in nephrotic syndrome or chronic liver disease
299
What is hemopericardium?
Accumulation of blood in pericardial sac
300
What causes hemopericardium?
Traumatic perforation of heart or aorta by myocardial rupture associated with MI
301
Five types of acute pericarditis?
1. Serous
2. Fibrinous/Serofibrinous
3. Purulent/Suppurative
4. Hemorrhagic
5. Caseous
302
Serous pericarditis is associated with what causes? (3)
1. SLE
2. Rheumatic fever
3. Viral infections
303
What is the liquid in acute pericarditis?
Protein-rich exudate with inflammatory cells
304
What is fibrinous/serofibrinous pericarditis characterized by?
Fibrin-rich exudate
305
What causes fibrinous/serofibrinous pericarditis? 5
1. uremia
2. Myocardial infarction
3. ARF
4. Dressler's syndrome
5. Radiation
306
What is clinical finding in fibrinous/serofibrinous pericarditis?
Loud friction rub
307
Purulent/suppurative pericarditis is characterized by what?
Inflammatory exudate
308
What causes purulent/suppurative pericarditis?
Bacterial infection
309
Hemorrhagic pericarditis is characterized by what?
Bloody inflammatory exudate
310
What causes hemorrhagic pericarditis? 2
1. Tumor invasion
2. TB or other bacterial infection
311
Overall, acute pericarditis presents how? 5
1. Sharp pain
2. Aggravated by inspiration
3. Relieved by sitting up and leaning forward
4. Friction rub
5. ST segment elevation or depression
312
Chronic pericarditis has what etiology? 2
1. TB
2. Pyogenic staph
313
Characteristics of chronic pericarditis? 4
1. Thickening and scarring of pericardium
2. Loss of elasticity
3. Mimics Right sided heart failure
4. Proliferation of fibrous tissue
314
Hypertrophy of left ventricle is caused by what? 2
HTN
Aortic or mitral valvular disease
315
Hypertrophy of right ventricle causes? 4
1. LV failure
2. Chronic lung disease
3. Mitral valve disease
4. Congenital heart disease with L-2-R shunt
316
Define cor pulmonale
Right ventircular hypertrophy secondary to prmary disease of pulmonary vasculature (P-HTN)
317
What is cardiac tamponade?
Compression of heart by fluid in pericardium --> leading to decreased cardiac output.
318