8. Heart 1 Flashcards
1
Q
What is the number 1 worldwide cause of mortality, causing 1/3 of deaths in the US?
A
Cardiovascular disease (CAD, stroke, peripheral vascular dz)
2
Q
The heart should weight approx 0.4-0.5% of the body. 250-320gm for females and 300-360gm for males. What are the right and left ventricle normal thicknesses?
A
Left ventricle 1.3-1.5cm
Right ventricle 0.3-0.5cm
3
Q
Hypertrophy of the heart is when there is an increase in ventricular thickness, cardiomegaly is when there is an increase in cardiac weight and dilation means?
A
enlarged chamber size
4
Q
Atrial myocytes have storage granules that contain atrial natriuretic peptide which promotes arterial vasodilation and stimulates what, which is beneficial in HTN and CHF?
A
renal salt and water elimnation (natriuresis and diuresis)
5
Q
Pathologic changes of valves are largely of 3 types… damage to collagen that weakens leaflets as seen in mitral prolapse, nodular calcification in interstitial cells as in calcific aortic stenosis (NOTCH 1) and?
A
fibrotic thickening as seen in rheumatic heart dz
6
Q
SA node is the pacemaker of the heart and the AV node is the gatekeeper of the heart which ensures?
A
that atrial contraction precedes ventricular systole
7
Q
LAD has diagnol branches and left circumflex A has marginal branches. When do the coronary arteries get their blood?
A
during ventricular diastole when the aortic valve closes, allowing blood flow to myocardium
8
Q
The cardiac stem cells are bone marrow derived precursors and stem cells present in the myocardium. Do the cells get replaced often?
A
NO! only 1% each year, so not able to recover from damage like other areas in the body
9
Q
As the heart ages the LV cavity/volume decreases while the walls thicken and there is an increase in epicardial fat, what can be seen histologically? 2
A
Lipofuscin and basophilic degeneration
10
Q
With age, aortic and mitral valves build annular calcification and fibrous thickening occurs. Mitral leaflets may buckle leading to what?
A
increase in left atrium size (d/t increased volume)
11
Q
what are small filiform processes that form on the closure lines of aortic and mitral valves probably resulting from the organization of small thrombi?
A
Lambl Excrescences
12
Q
What occurs when the myocardium contracts weakly during systole and there is inadequate cardiac output OR myocardium may relax insufficiently during diastole to permit adequate ventricular filling?
A
Pump failure
13
Q
Another cardiac pathophysiology mechanism that can occur are lesions can obstruct blood flow through a vessel or prevent valve opening or otherwise increased ventricular chamber pressure… known as?
A
flow obstruction
14
Q
What occurs when a portion of the output from each contraction flows backward through an incompetent valve, adding a volume overload to the affected atria or ventricles?
A
Regurgitation flow
15
Q
What occurs when blood is diverted from one part of the heart to another thorugh defects that can be congenital or acquired?
A
Shunted flow
16
Q
What is the most common cardiac pathophys when conduction defects or arrhythmias due to uncoordinated generation or transmission of impulses lead to nonuniform and inefficient myocardial contrations - fatal?
A
disorders of cardiac confuction
17
Q
What occurs in situations there is cataclysmic exsanguination either into body cavities or externally?
A
rupture of the heart or a major vessel
18
Q
What occurs when the heart is unable to pump blood at a rate to meet peripheral demand or can only do so with increased filling pressure?
A
Congestive heart failure CHF
19
Q
CHF may results from loss of myocardial contractile function (systolic dysfunction) or from loss of ability to?
A
fill the ventricles during diastole (diastole dysfunction
20
Q
Cardiac myocytes become hypertrophic when there is sustained pressure or volume overload due to systemic HTN or aortic stenosis or when there is sustained?
A
trophic signals such as B-adrenergic stimulation
21
Q
In the setting of pressure overload hypertrophy, the myocytes become thicker and?
A
the left ventricle increases thickness concentrically (cause need stronger contraction to beat high pressure)
22
Q
In the setting of volume overload hypertrophy, myocytes elongate resulting in?
A
ventricular dilation
23
Q
What is the best measure of hypertrophy in a dilated heart?
A
the heart weight
24
Q
The hypertrophied heart is not accompanied by increase in blood supply despite the inc. in energy demand, making the heart vulnerable to?
A
ischemia-related decompensation
25
What mechanism is in which increased filling volumes dilate the heart and thereby increases subsequent actin-myosin cross bridge formation, enhancing contractility and stroke volume?
Frank-Starling mechanism
26
Left-sided heart failure can be systolic or diastolic failure and most common a result of left sided valve disease, primary myocardial disease and what other 2?
myocardial ischemia
| hypertension**
27
Forward failure is when there are variable degrees of decreased cardiac output and tissue perfusion. What is backward failure?
pooling of blood in the venous capacitance system (lead to pulmonary edema)
28
Clinical effects of left sided heart failure are due to congestion in the pulmonary circulation and decreased perfusion. The morphology of the heart is usually one of two things?
LV is hypertrophied or dilated massively
29
LV dysfunction leads to L atrial dilation which can lead to thrombus and what else?2
stasis and atrial fibirillation
30
Left sided HF can also cause pulmonary congestion and edema which cause 1) Kerley B and C lines on Xray, 2) progressive edematous widening of alverolar septa and 3) (most severe)?
accumulation of edema fluid in alveolar space
31
Common symptoms of left sided HF are mild pulmonary sxs: cough, dyspnea, orthopnea (breathing laying down), paroxysmal nocturnal dyspnea and what else? 2
atrial fibirillation
| tachycardia (cyanosis)
32
L sided HF results in decreased ejection fraction which results in decreased glomerular perfusion causing what? 2
```
stimulating release of renin to inc. volume
prerenal azotemia (dec. NO filtration)
```
33
Advanced Lsided HF may lead to decreased cerebral perfusion resulting in?
Hypoxic encephalopathy
34
Histologically, what is unique to Left sided heart failure which is a common sign of pulomnary edema? ***IMP
Heart failure cells = hemosiderin-laden macrophages (phagocytosed RBD in edema fluid in lungs)
35
Diastolic Left sided Heart failure is more common in who?
women over the age of 65
| HTN, diabetes, obesity
36
What is the most common cause of right sided heart failure?
left sided heart failure
37
When there is right sided HF alone (cor pulmonale), with out the left side, it results from any cause of?
pulmonary hypertension
38
Some common causes of pulm. HTN include parenchymal lunch dz, primary pulmonary HTN, and ?
pulmonary vasconstriction
39
In primary right sided HF, pulmonary congestion is minimal (none) and the VENOUS system is markedly congested, what are three types of edema that can be seen due to this?
Liver congestionn (NUTMEG LIVER)
Splenic congestion/splenomegaly
Ankles/peritibial edema (ansacara massive generalized edema)
40
With right sided HF, ascites can be seen, along with effusions involving peritonea, pleural and pericardial spaces. What can be seen in the kidneys?
renal congestion, causing dec BF through kidneys = worsening azotemia
41
Sporadic genetic abnormalities are the major known causes of?
congenital heart dz (seen in turner syndrome, trisomies 13,18,21)
42
The single most common genetic cause of congenital heart diesase is ?
Trisomy 21 (40% of patients with downs have at least one heart defect)
43
Down syndrome heart defect usually are derived from the second heart filed (atrioventricular septae) and most commonly defects of the endocardial cushion including? 4
ostium primum
ASDs
AV Valve malformations
VSDs ***MC in live births
44
Notch pathway are associated with a variety of congenital heart defects, including bicuspid aortic valve and tetrology of fallot with what gene relations?
Bicuspid aortic valve (NOTCH1)
| Tetralogy of Fallot (JAG1/NOTCH2)
45
DiGeorge Syndrome (22q11.2) can be remembered by CATCH22, meaning?
```
cardiac abnormality
abnormal facies
thymic aplasia
cleft palate
hypocalcemia (on chr 22)
```
46
The most common congenital heart disease is a left to right shunt, which inlcude what 3 which all have D in the acronym?
ASD
VSD
PDA (patent ductus arteriosus)
47
In ASD there is an increase in only right ventricle and pulmonary outflow volumes while VSD and PDA cause what?
and increase in pulmonary blood flow AND pressure
48
Do left to right shunts (ASD VSD PDA) usually have cyanosis?
NO! not initially associated with cyanosis
49
ASDs are usually asymptomatic until adulthood (>30y/o). What accounts for 90% of alll ASD, located in the center of the atrial septum which may be multiple or fenestrated?
Secundum ASD
50
What defect acounts for 5% of all ASDs usually adjacent to AV valves and associated with AV valve abnormalities and or VSD?
Primum anomalie
51
What is a very rare ASD, near entrance of superior vena cava and can be associated with anomalous pulmonary venous return to the right atrium?
Sinus venosa defects
52
Left to right shunting causes volume overload on the right side which may lead to pulmonary HTN, paradoxical embolization and right heart failure and may be closed how?
surgically with normal survival
53
80% of patent foramen ovale PFO closes permanently by 2 years of age, while the remaining 20% can open if?
there is an increase in right side pressure
54
Even temporary increased pressure can produce breif periods of R-L shunting, including? 3
Pulmonary HTN
Bowel Movement
Coughing/Sneezing
55
Why are paradoxical embolus common in PFOs?
If you are a drug addict and have a PFO, you get valve vegitations on tricuspid that break off and go from right to left atrium to the brain
56
The most common form of congeital heart disease, wiith 90% of them occuring in membranous interventricular septum are?
Ventricular Septal Defects (VSDs)
90% are membranous VSDs
57
What type of VSD is found below the pulmonary valve or within the muscular septum?
Infundibular VSD (may be multiple here)
58
The effects of VSD depend on the size and presence of other heart defects.. those that manifest with sx as children usually are associated with?
Tetralogy of Fallot
59
Large VSDs may cause significant shunting leading to right ventricular hypertrophy and pulmonary HTN. Unclosed large VSDs can lead to?
shunt reversal, leading to cyanosis and death
60
What may fail to close when infants are hypoxic and or have defects associated with increased pulmonary vascular pressure (VSDs)?
Ductus arteriosus (Patent) PDA (between pulmonary A and aorta)
61
PDAs are (Left to right shunt) are usually asymptomatic at birth, and usually no cyanosis. They produce what type of murmur?
Harsh, machinery like murmur
62
The effect of a PDA is determined by the shunts diameter, large shunts can icnrease pulmonary pressure and eventually cause?
shunt reversal (R2L) and cyanosis
63
Isolated PDAs should be closed immediately, but what may be given to keep a PDA open in the case of an aortic valve atresia, saving the newborn?
Prostaglandin E2 PGE2 - which keeps the PDA open
64
Right to left shunts cause cyanosis early in postnatal life ***cyanotic congenital heart dz. What are the 5 examples? (all have T in them)
```
Right to Left shunting
Tetralogy of Fallot (TOF) **MOST COMMON
Transposition of the great arteries
Persistent Truncus arteriosus
Tricuspid Atresia
Total anomalous pulmonary venous connection
```
65
What are the four cardinal features associated with right to left shunt tetralogy of fallot (TOF)?
1. VSD
2. Obstruction of RV outflow tract (pulmonary trunk)
3. Aorta overrides teh VSD
4. Right ventricular hypertrophy
66
What defect makes the heart enlarged and boot shaped because of the right ventricular hypertrophy?
Tertalogy of Fallot (caused by anterior superior displacement of infundibular septum)
67
The clinical severity of TOF depends on the degree of subpulmonary stenosis... mild stenosis there is a shunt from L to R via VSD (pink tetralogy)... in classic TOF...?
R to L shunting with cyanosis - most children from birth are cyanotic
**overriding aorta
68
What are the four clinical symptoms of TOF?
squatting
cyanosis
clubbing of fingers
syncope
69
Transposition of the great vessels (TGA) results in two separate systemic and pulmonary circulations which is incompatible with life after birth unless?
a shunt is present for mixing of blood from the two circulations (PDA)
70
1/3 of TGAs have a VSD, 2/3 have a PDA. What occurs to the left and right ventricles?
The right ventricle hypertrophies because it is supplying the system and the left ventricle atrophies since it is pumping to the pulmonary circuit
71
What does a tricuspid atresia patient require in order to survive before surgery?
ASD and VSD- patients cyanotic from birth with high mortality
72
What is narrowing of the aorta, generally seen with a PDA or without a PDA(adult form)?
Coarctation of the Aorta (more common in Turner syndrome, males 2x females)
73
The clinical severity depends on the degree of narrowing in coarctation and patency of the ductus arteriosus. What is unique about the cyanosis in coarctation of the aorta WITH PDA??
may produce cyanosis in the lower half of the body (because not able to pump blood far)
74
Coarctation without PDA is usually asymptomatic, and will see hypertension in the UE and hypotension in the LE. What other 2 things can be seen?
Claudication (pain) and cold LE
| Eventually-Concentric LV hypertrophy
75
Coarctation with PDA is after the stenosis while without PDA, the coarctation is distal to the arch. Why can one see rib notching in someone without PDA?
collateral circulation through intercostal/internal mammary arteries supply organs distal to the coarctation
76
What type of murmur can be heart with coarctation?
Throughout systole +/- vibratory thrill
77
What syndrome is most often a complication of having a hole (shunt) between two chambers of your heart? (left to right shunts)
Eisenmenger syndrome
78
Eventually the shunt irreparable damages the walls of your lung's arteries and E syndrome occurs when the pressure in the pulmonary arteries is so high that is causes oxygen poor blood to?
flow from the right to left ventricle (instead of left to right) and then to the body, causing cyanosis (shunt reversal?)
79
The following are associated with what? polycythemia, hypertrophic osteoarthropathy, and paradoxical emboli
Right to left shunts (TOF TGA)
80
What results from insufficient perfusion to meet the metabolic demands of the myocardium?
Ischemic heart dz
81
Blood is supplied to the myocardium via coronary arteries, so any disruption of coronary flow may result in ischemia. What are the four main consequences of ischemia?
MI
Angina pectosi (chest pain without heart attack)
Chronic ischemia dz with HF
Sudden cardiac death
82
Ischemic heart dz is the leading cause of death in the us and more than 90% are secondary to?
athersclerosis
| chronic vascular occlusion, acute plaque change (thrombus)
83
What is transient, recurrent chest pain induced by myocardial ischemia insufficient to induce myocardial infarction?
Angina Pectoris
84
What are the 3 clinical stages of angina pectoris?
stable angina
Prinzmetal variant angina
Unstable (crescendo) angina
85
Stable angina is the MC form and is due to stenotic occlusion of the coronary artery. A pt can feel squeezin or burning sensation relieved by rest or vasodilators... what is the pain usually induced by? 2
physical activity
| stress
86
What type of angina causes episodic attacks due to coronary artery spasm relived with vasodilators, UNRELATED to physical activity, HR or BP?
Prinzmetal variant angina
87
Unstable angina is frank pain, increasing in frequency (crescendo), duration and severity... Common at low levels of activity and eventually even at rest. What usually happens?
rupture of athersclerotic plaque with partial thrombus
*50% have evidence of myocardial necrosis (ACUTE MI MAY BE IMMINENT)
88
MI age distribution and risk factors mirror those of atherosclerosis becuase nearly 90% are caused by?
an atheromatous plaque
89
The other 10% that causes MIs include embolus, vasospasms, and ischemia secondary to?
vasculitis, schock or hematologic abnormalities
90
The classic presentation of an MI is men not women, with prolonged chest pain greater than 30 minutes (crushing/stabbing/tightness radiating down left arm/left jaw), and what other 3 sx?
DIAPHORESIS
Dyspnea
Nausea-vomitting
*note: 25% asymptomatic
91
The location size and features of an acute MI depond on the site degree and rate of occlusion of the artery, size of area perfused, duration of occlusion, metabolic/oxygen needs of area and what else? 2
extent of collateral blood flood (usually no collaterals in heart)
presence of arterial spasm
92
Following a severe myocardial ischemia, early changes (within 30 minutes) includ loss of ATP and accumulation of lactate (often irreversible). If it is caught within 30 minutes, what can happen?
myocardial injury is potentially irreversible, with benefits of reperfusion achieved early, thereafter loss of viability is complete by 6-12 hrs
93
Irreversible cell injury occurs at 20-40 minutes while microvascular injury occurs at?
greater than 1 hour
94
Necrosis after coronary artery occlusion begins in a small zone of the myocardium beneath the endocardial surface in the center of the ischemic zone. Why?
it is the area furthest away from the blood supply.. Note: the myocardium directly beneath the endocardium is saved d/t it being oxygenated via diffusion from the ventricle
95
The Left anterior descending artery is infarcted 40-50% of the time and supplies what regions? 3
Most of the apex
anterior wall of the LV
Anterior 2/3 of the ventricular septum
96
The right coronary A is infarcted 30-40% of the time and supplies what regions? 3
Right ventricular free wall
left ventricular posterior wall
posterior 1/3 of the ventricular septum
97
The left circumflex A is infarcted 15-20% of the time and supplies what regions of the heart? 1
Left ventricular lateral wall
98
What type of MI occurs when it is complete thickness, meaning across the wall from subendocardium to subepicardium, representing a long standing severe ischemia?
Transmural MI ( sometimes called a STEMI) caused by completely occuding thrombosis/stenosis
99
Non-transmural (sunendocardial) infarcts refers to?
Infarcts that do no go from subendocardium to subepicardium, partial infarcts when there is not full occlusion
100
Transient/partial obstruction of a coronary artery results in?
regional subendocardial infarct
101
Global hypotension (affecting all coronary arteries) results in?
circumferential subendocardial infarct
102
Small intramural vessel occlusions results in what type of infarct?
microinfarcts
103
What can be seen grossly from 0-18hours?
NO change
104
What can be seen grossly from 18-24hrs?
Dark mottling
105
What can be seen grossly from 1-3days?
Yellow tan center of mottling
106
What can be seen grossly from 3-7 days post MI?
yellow tan center with hyperemic border
107
What can be seen grossly from 7-10 days?
max ywellow tan, soft, depressed red tan margins
108
What can be seen grossly from 10-14 days?
red-grey depressed infarct borders
109
What can be seen grossly from 2-8weeks?
white grey firm scar that progresses in from border to center
110
What can be seen grossly from 2 months?
scarring complete, dense fibrous scar of 8wk and 10 wk look same
111
What can be seen histologically 1/2-4hrs post MI?
None, wavy fibers at border
112
What can be seen histologically 4-12hrs post MI?
early coagulative necrosis, edema, hemorrhage
113
What can be seen histologically 12-24hrs post MI?
ongoing coagulative necrosis, pyknosis of nuclei, nuclei hyper-eosinophilla, marginal contraction of band necrosis, early neutrophil infiltrate
114
What can be seen histologically 1-3 days post MI?
coagulative necrosis w neutrophils, loss of nuclei/striations
115
What can be seen histologically 3-7 days post MI?
coagulative necrosis with mø, dying neutrophils, first time the dead myofibers are being eaten
116
What can be seen histologically 10-14 days post MI?
granulation tissue with new BV and collagen deposition
117
What can be seen histologically 2-8 weeks post MI?
increased collagen, decreased cells (after 2 months dense collagenous scar)
118
Reperfusion is the restoration of blood flow to ischemic myocadium threatened by infarction; the goal is to?
salvage cardiac muscle at risk and limit infarct size
119
What are the 4 main procedures done to enact prompt reperfusion after an MI?
Thrombolytics
Angioplasty
Stent placement
coronary artery bypass graft CABG
120
If reperfusion is done in less than 40 mins = complete recovery tissue, if done at 2-4 hours, necrosis of subendocardium and rescue of surrounding tissue... If done at greater than 6 hours, what may happen?
may be hazardous will not improve infarct size
121
Reperfusion grossly, you can see large densely hemorrhagic myocardium, what can be seen histologically after reperfusion injury?
contraction bands which are eosinophillic intracellular strips compased of closely packed sarcomeres (d/t large amt Ca+ - seen in irreversibly injured myocytes) also can see necrosis hemorrhage
122
When there is permanent occlusion with no blood flow restored, viability and function is 0% of the original. When there is temporary occlusion with reperfusion, myocardial tissue function is saved and?
viability is saved as well, however it comes at a cost, and reperfusion injury causes some damage as well- but youre not dead at least!
123
An MI is diagnosed by clinical symptoms, laboratory tests for the presence of myocardial proteins in the plasma and characteristic ECG changes. The lab evaluation of MI is based on measuring?
blood levels of proteins that leak out of irreversibly damaged myocytes
(most useful being cardiac specific troponins cTnT and cTnI and the CKMB)
124
Cardiac troponins are the gold standard, they begin to appear at 3-12 hours, when do cTnT and cTnI peak?
cTnT at 12-48 hours done by 5-14 days
| cTnI at 24 hours normal at 5-10d
125
Why is CKMB no longer the gold standard for MIs?
it is sensitive but not specific (can be elevated after skeletal muscle injury)
126
What are the steps post MI of the release of myocyte proteins? 2
1. Plasma membrane of necrotic myocytes become leaky
| 2. CKMB/Troponin leak out of cell into circ
127
What are proteins that regulate calcium-mediated contraction of cardiac and skeletal muscle?
Troponin
128
CKMB beings to rise 3-12hrs post MI and peaks at about 24 hours, lasting for?
48-72hours
129
Arrhythmia is a complication of MI, half of all MI deaths occur within 1 hour of onset and are usually secondary to?
an arrhythmia!
130
Arrhythmia is a complication of MI, half of all MI deaths occur within 1 hour of onset and are usually secondary to?
an arrhythmia!
131
Arrhythmia can be can be a longer term complication of MI depending on the site and extent of the lesion, can result from?2
permanent damage to the conducting system
| or from myocardial irritability follow infarct
132
What dysfunction post MI is proportional to the size of the infarct that leads to hypotension, pulmonary vascular congestion and respiratory impairment?
Contractile dysfunction
133
A fibrinous pericarditis develops 2-3 days after a transmural infarct as a result of?
underlying myocardial inflammation (bread and butter)
134
What is a complication of an MI that requires a transmural infarct and occurs 2-4 days post MI when inflammation and necrosiss have weakened the wall?
Myocardial rupture (ventricular free wall most common)
135
What are some risk factors for myocardial rupture? 4
increased age
large TRANSMURAL anterior MI
first MI
absence of LV hypertrophy
136
What is a late complication of large transmural infarcts with early expansion, which is composed of a thin wall of scarred myocardium and is also associated with mural thrombus?
Ventricular Aneurysm (rupture doesnt usually occur)
137
What is progressive congestive heart failure as a consequence of accumulated ischemic myocardial damage either from prior infarctions or chronic low grade ischemia?
Chronic Ischemic Heart Disease IHD
138
Chronic IHD patients account for 50% of all heart transplant recipients. What is typically seen in hearts with C IHD?
```
cardiomegaly w LV hypertrophy/dilation
stenotic coronary athersclerosis
scars from old MIs
Patchy fibrous thickenings
Mural thrombi
subendocardial vacuolization and fibrosis
```
