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21. CPR Exam 1 > 8. Heart 1 > Flashcards

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)

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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

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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

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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)

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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

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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

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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

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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

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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

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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)

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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)

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22
Q

In the setting of volume overload hypertrophy, myocytes elongate resulting in?

A

ventricular dilation

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23
Q

What is the best measure of hypertrophy in a dilated heart?

A

the heart weight

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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

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25
Q

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?

A

Frank-Starling mechanism

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26
Q

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?

A

myocardial ischemia

hypertension**

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27
Q

Forward failure is when there are variable degrees of decreased cardiac output and tissue perfusion. What is backward failure?

A

pooling of blood in the venous capacitance system (lead to pulmonary edema)

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28
Q

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?

A

LV is hypertrophied or dilated massively

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29
Q

LV dysfunction leads to L atrial dilation which can lead to thrombus and what else?2

A

stasis and atrial fibirillation

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30
Q

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)?

A

accumulation of edema fluid in alveolar space

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31
Q

Common symptoms of left sided HF are mild pulmonary sxs: cough, dyspnea, orthopnea (breathing laying down), paroxysmal nocturnal dyspnea and what else? 2

A

atrial fibirillation

tachycardia (cyanosis)

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32
Q

L sided HF results in decreased ejection fraction which results in decreased glomerular perfusion causing what? 2

A 
stimulating release of renin to inc. volume
prerenal azotemia (dec. NO filtration)
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33
Q

Advanced Lsided HF may lead to decreased cerebral perfusion resulting in?

A

Hypoxic encephalopathy

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34
Q

Histologically, what is unique to Left sided heart failure which is a common sign of pulomnary edema? ***IMP

A

Heart failure cells = hemosiderin-laden macrophages (phagocytosed RBD in edema fluid in lungs)

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35
Q

Diastolic Left sided Heart failure is more common in who?

A

women over the age of 65

HTN, diabetes, obesity

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36
Q

What is the most common cause of right sided heart failure?

A

left sided heart failure

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37
Q

When there is right sided HF alone (cor pulmonale), with out the left side, it results from any cause of?

A

pulmonary hypertension

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38
Q

Some common causes of pulm. HTN include parenchymal lunch dz, primary pulmonary HTN, and ?

A

pulmonary vasconstriction

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39
Q

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?

A

Liver congestionn (NUTMEG LIVER)
Splenic congestion/splenomegaly
Ankles/peritibial edema (ansacara massive generalized edema)

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40
Q

With right sided HF, ascites can be seen, along with effusions involving peritonea, pleural and pericardial spaces. What can be seen in the kidneys?

A

renal congestion, causing dec BF through kidneys = worsening azotemia

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41
Q

Sporadic genetic abnormalities are the major known causes of?

A

congenital heart dz (seen in turner syndrome, trisomies 13,18,21)

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42
Q

The single most common genetic cause of congenital heart diesase is ?

A

Trisomy 21 (40% of patients with downs have at least one heart defect)

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43
Q

Down syndrome heart defect usually are derived from the second heart filed (atrioventricular septae) and most commonly defects of the endocardial cushion including? 4

A

ostium primum
ASDs
AV Valve malformations
VSDs ***MC in live births

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44
Q

Notch pathway are associated with a variety of congenital heart defects, including bicuspid aortic valve and tetrology of fallot with what gene relations?

A

Bicuspid aortic valve (NOTCH1)

Tetralogy of Fallot (JAG1/NOTCH2)

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45
Q

DiGeorge Syndrome (22q11.2) can be remembered by CATCH22, meaning?

A 
cardiac abnormality
abnormal facies
thymic aplasia
cleft palate
hypocalcemia (on chr 22)
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46
Q

The most common congenital heart disease is a left to right shunt, which inlcude what 3 which all have D in the acronym?

A

ASD
VSD
PDA (patent ductus arteriosus)

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47
Q

In ASD there is an increase in only right ventricle and pulmonary outflow volumes while VSD and PDA cause what?

A

and increase in pulmonary blood flow AND pressure

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48
Q

Do left to right shunts (ASD VSD PDA) usually have cyanosis?

A

NO! not initially associated with cyanosis

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49
Q

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?

A

Secundum ASD

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50
Q

What defect acounts for 5% of all ASDs usually adjacent to AV valves and associated with AV valve abnormalities and or VSD?

A

Primum anomalie

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51
Q

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?

A

Sinus venosa defects

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52
Q

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?

A

surgically with normal survival

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53
Q

80% of patent foramen ovale PFO closes permanently by 2 years of age, while the remaining 20% can open if?

A

there is an increase in right side pressure

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54
Q

Even temporary increased pressure can produce breif periods of R-L shunting, including? 3

A

Pulmonary HTN
Bowel Movement
Coughing/Sneezing

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55
Q

Why are paradoxical embolus common in PFOs?

A

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

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56
Q

The most common form of congeital heart disease, wiith 90% of them occuring in membranous interventricular septum are?

A

Ventricular Septal Defects (VSDs)

90% are membranous VSDs

57
Q

What type of VSD is found below the pulmonary valve or within the muscular septum?

A

Infundibular VSD (may be multiple here)

58
Q

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?

A

Tetralogy of Fallot

59
Q

Large VSDs may cause significant shunting leading to right ventricular hypertrophy and pulmonary HTN. Unclosed large VSDs can lead to?

A

shunt reversal, leading to cyanosis and death

60
Q

What may fail to close when infants are hypoxic and or have defects associated with increased pulmonary vascular pressure (VSDs)?

A

Ductus arteriosus (Patent) PDA (between pulmonary A and aorta)

61
Q

PDAs are (Left to right shunt) are usually asymptomatic at birth, and usually no cyanosis. They produce what type of murmur?

A

Harsh, machinery like murmur

62
Q

The effect of a PDA is determined by the shunts diameter, large shunts can icnrease pulmonary pressure and eventually cause?

A

shunt reversal (R2L) and cyanosis

63
Q

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?

A

Prostaglandin E2 PGE2 - which keeps the PDA open

64
Q

Right to left shunts cause cyanosis early in postnatal life ***cyanotic congenital heart dz. What are the 5 examples? (all have T in them)

A 
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
Q

What are the four cardinal features associated with right to left shunt tetralogy of fallot (TOF)?

A
  1. VSD
  2. Obstruction of RV outflow tract (pulmonary trunk)
  3. Aorta overrides teh VSD
  4. Right ventricular hypertrophy
66
Q

What defect makes the heart enlarged and boot shaped because of the right ventricular hypertrophy?

A

Tertalogy of Fallot (caused by anterior superior displacement of infundibular septum)

67
Q

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…?

A

R to L shunting with cyanosis - most children from birth are cyanotic

**overriding aorta

68
Q

What are the four clinical symptoms of TOF?

A

squatting
cyanosis
clubbing of fingers
syncope

69
Q

Transposition of the great vessels (TGA) results in two separate systemic and pulmonary circulations which is incompatible with life after birth unless?

A

a shunt is present for mixing of blood from the two circulations (PDA)

70
Q

1/3 of TGAs have a VSD, 2/3 have a PDA. What occurs to the left and right ventricles?

A

The right ventricle hypertrophies because it is supplying the system and the left ventricle atrophies since it is pumping to the pulmonary circuit

71
Q

What does a tricuspid atresia patient require in order to survive before surgery?

A

ASD and VSD- patients cyanotic from birth with high mortality

72
Q

What is narrowing of the aorta, generally seen with a PDA or without a PDA(adult form)?

A

Coarctation of the Aorta (more common in Turner syndrome, males 2x females)

73
Q

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??

A

may produce cyanosis in the lower half of the body (because not able to pump blood far)

74
Q

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?

A

Claudication (pain) and cold LE

Eventually-Concentric LV hypertrophy

75
Q

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?

A

collateral circulation through intercostal/internal mammary arteries supply organs distal to the coarctation

76
Q

What type of murmur can be heart with coarctation?

A

Throughout systole +/- vibratory thrill

77
Q

What syndrome is most often a complication of having a hole (shunt) between two chambers of your heart? (left to right shunts)

A

Eisenmenger syndrome

78
Q

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?

A

flow from the right to left ventricle (instead of left to right) and then to the body, causing cyanosis (shunt reversal?)

79
Q

The following are associated with what? polycythemia, hypertrophic osteoarthropathy, and paradoxical emboli

A

Right to left shunts (TOF TGA)

80
Q

What results from insufficient perfusion to meet the metabolic demands of the myocardium?

A

Ischemic heart dz

81
Q

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?

A

MI
Angina pectosi (chest pain without heart attack)
Chronic ischemia dz with HF
Sudden cardiac death

82
Q

Ischemic heart dz is the leading cause of death in the us and more than 90% are secondary to?

A

athersclerosis

chronic vascular occlusion, acute plaque change (thrombus)

83
Q

What is transient, recurrent chest pain induced by myocardial ischemia insufficient to induce myocardial infarction?

A

Angina Pectoris

84
Q

What are the 3 clinical stages of angina pectoris?

A

stable angina
Prinzmetal variant angina
Unstable (crescendo) angina

85
Q

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

A

physical activity

stress

86
Q

What type of angina causes episodic attacks due to coronary artery spasm relived with vasodilators, UNRELATED to physical activity, HR or BP?

A

Prinzmetal variant angina

87
Q

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?

A

rupture of athersclerotic plaque with partial thrombus

*50% have evidence of myocardial necrosis (ACUTE MI MAY BE IMMINENT)

88
Q

MI age distribution and risk factors mirror those of atherosclerosis becuase nearly 90% are caused by?

A

an atheromatous plaque

89
Q

The other 10% that causes MIs include embolus, vasospasms, and ischemia secondary to?

A

vasculitis, schock or hematologic abnormalities

90
Q

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?

A

DIAPHORESIS
Dyspnea
Nausea-vomitting

*note: 25% asymptomatic

91
Q

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

A

extent of collateral blood flood (usually no collaterals in heart)
presence of arterial spasm

92
Q

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?

A

myocardial injury is potentially irreversible, with benefits of reperfusion achieved early, thereafter loss of viability is complete by 6-12 hrs

93
Q

Irreversible cell injury occurs at 20-40 minutes while microvascular injury occurs at?

A

greater than 1 hour

94
Q

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?

A

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
Q

The Left anterior descending artery is infarcted 40-50% of the time and supplies what regions? 3

A

Most of the apex
anterior wall of the LV
Anterior 2/3 of the ventricular septum

96
Q

The right coronary A is infarcted 30-40% of the time and supplies what regions? 3

A

Right ventricular free wall
left ventricular posterior wall
posterior 1/3 of the ventricular septum

97
Q

The left circumflex A is infarcted 15-20% of the time and supplies what regions of the heart? 1

A

Left ventricular lateral wall

98
Q

What type of MI occurs when it is complete thickness, meaning across the wall from subendocardium to subepicardium, representing a long standing severe ischemia?

A

Transmural MI ( sometimes called a STEMI) caused by completely occuding thrombosis/stenosis

99
Q

Non-transmural (sunendocardial) infarcts refers to?

A

Infarcts that do no go from subendocardium to subepicardium, partial infarcts when there is not full occlusion

100
Q

Transient/partial obstruction of a coronary artery results in?

A

regional subendocardial infarct

101
Q

Global hypotension (affecting all coronary arteries) results in?

A

circumferential subendocardial infarct

102
Q

Small intramural vessel occlusions results in what type of infarct?

A

microinfarcts

103
Q

What can be seen grossly from 0-18hours?

A

NO change

104
Q

What can be seen grossly from 18-24hrs?

A

Dark mottling

105
Q

What can be seen grossly from 1-3days?

A

Yellow tan center of mottling

106
Q

What can be seen grossly from 3-7 days post MI?

A

yellow tan center with hyperemic border

107
Q

What can be seen grossly from 7-10 days?

A

max ywellow tan, soft, depressed red tan margins

108
Q

What can be seen grossly from 10-14 days?

A

red-grey depressed infarct borders

109
Q

What can be seen grossly from 2-8weeks?

A

white grey firm scar that progresses in from border to center

110
Q

What can be seen grossly from 2 months?

A

scarring complete, dense fibrous scar of 8wk and 10 wk look same

111
Q

What can be seen histologically 1/2-4hrs post MI?

A

None, wavy fibers at border

112
Q

What can be seen histologically 4-12hrs post MI?

A

early coagulative necrosis, edema, hemorrhage

113
Q

What can be seen histologically 12-24hrs post MI?

A

ongoing coagulative necrosis, pyknosis of nuclei, nuclei hyper-eosinophilla, marginal contraction of band necrosis, early neutrophil infiltrate

114
Q

What can be seen histologically 1-3 days post MI?

A

coagulative necrosis w neutrophils, loss of nuclei/striations

115
Q

What can be seen histologically 3-7 days post MI?

A

coagulative necrosis with mø, dying neutrophils, first time the dead myofibers are being eaten

116
Q

What can be seen histologically 10-14 days post MI?

A

granulation tissue with new BV and collagen deposition

117
Q

What can be seen histologically 2-8 weeks post MI?

A

increased collagen, decreased cells (after 2 months dense collagenous scar)

118
Q

Reperfusion is the restoration of blood flow to ischemic myocadium threatened by infarction; the goal is to?

A

salvage cardiac muscle at risk and limit infarct size

119
Q

What are the 4 main procedures done to enact prompt reperfusion after an MI?

A

Thrombolytics
Angioplasty
Stent placement
coronary artery bypass graft CABG

120
Q

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?

A

may be hazardous will not improve infarct size

121
Q

Reperfusion grossly, you can see large densely hemorrhagic myocardium, what can be seen histologically after reperfusion injury?

A

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
Q

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?

A

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
Q

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?

A

blood levels of proteins that leak out of irreversibly damaged myocytes

(most useful being cardiac specific troponins cTnT and cTnI and the CKMB)

124
Q

Cardiac troponins are the gold standard, they begin to appear at 3-12 hours, when do cTnT and cTnI peak?

A

cTnT at 12-48 hours done by 5-14 days

cTnI at 24 hours normal at 5-10d

125
Q

Why is CKMB no longer the gold standard for MIs?

A

it is sensitive but not specific (can be elevated after skeletal muscle injury)

126
Q

What are the steps post MI of the release of myocyte proteins? 2

A
  1. Plasma membrane of necrotic myocytes become leaky

2. CKMB/Troponin leak out of cell into circ

127
Q

What are proteins that regulate calcium-mediated contraction of cardiac and skeletal muscle?

A

Troponin

128
Q

CKMB beings to rise 3-12hrs post MI and peaks at about 24 hours, lasting for?

A

48-72hours

129
Q

Arrhythmia is a complication of MI, half of all MI deaths occur within 1 hour of onset and are usually secondary to?

A

an arrhythmia!

130
Q

Arrhythmia is a complication of MI, half of all MI deaths occur within 1 hour of onset and are usually secondary to?

A

an arrhythmia!

131
Q

Arrhythmia can be can be a longer term complication of MI depending on the site and extent of the lesion, can result from?2

A

permanent damage to the conducting system

or from myocardial irritability follow infarct

132
Q

What dysfunction post MI is proportional to the size of the infarct that leads to hypotension, pulmonary vascular congestion and respiratory impairment?

A

Contractile dysfunction

133
Q

A fibrinous pericarditis develops 2-3 days after a transmural infarct as a result of?

A

underlying myocardial inflammation (bread and butter)

134
Q

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?

A

Myocardial rupture (ventricular free wall most common)

135
Q

What are some risk factors for myocardial rupture? 4

A

increased age
large TRANSMURAL anterior MI
first MI
absence of LV hypertrophy

136
Q

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?

A

Ventricular Aneurysm (rupture doesnt usually occur)

137
Q

What is progressive congestive heart failure as a consequence of accumulated ischemic myocardial damage either from prior infarctions or chronic low grade ischemia?

A

Chronic Ischemic Heart Disease IHD

138
Q

Chronic IHD patients account for 50% of all heart transplant recipients. What is typically seen in hearts with C IHD?

A 
cardiomegaly w LV hypertrophy/dilation
stenotic coronary athersclerosis
scars from old MIs
Patchy fibrous thickenings
Mural thrombi
subendocardial vacuolization and fibrosis

21. CPR Exam 1 (26 decks)

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