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CPR 2 Exam 1 > Cardiac Pathology 1 > Flashcards

Cardiac Pathology 1 Flashcards

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
Q

When is shunting of blood seen?

A

VSD
PDA
After MI

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26
Q

What is the most common cause of death in the first 24 hours after infarction?

A

Arrhythmias

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27
Q

How does ischemic injury cause arrhythmias?

A

Ischemic injury -> cardiac remodeling -> increased fibrosis -> dilated cardiac dysfunction -> arrhythmias

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28
Q

When does traumatic aortic dissection frequently occur?

A

MVC

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29
Q

What happens with aortic dissection due to MVC?

A

Rapid deceleration forces causes blow to the chest as the steering wheel impacts the driver -> traumatic separation of ligmentum arteriosum from aorta

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30
Q

When does abnormal dilation of a heart chamber occur?

A

Volume overload

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31
Q

When does hypertrophy occur?

A

Increase in pressure

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32
Q

Increased pressure causes what type of hypertrophy?

A

Concentric

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33
Q

Increased volume causes what type of hypertrophy?

A

Eccentric

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34
Q

In dilated hearts how is hypertrophy measured?

A

Heart weight

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35
Q

What happens to myocytes in concentric hypertrophy?

A

Increase in size or diameter of myocytes

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36
Q

What happens to myocytes in eccentric hypertrophy?

A

Increase in length

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37
Q

What causes left ventricular hypertrophy?

A

Chronic HTN

Aortic valvular stenosis

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38
Q

Overload of what causes cardiac dysfunction and heart failure?

A

Pressure

Volume

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39
Q

Is there an increase in capillary number with pathologic hypertrophy?

A

No

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40
Q

Is there an increase in capillary number in exercise induced hypertrophy?

A

Yes

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41
Q

Why does hypertrophy lead to ischemic decompensation

A

No additional capillaries but increased oxygen required

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42
Q

What happens with increased activity of the neurohumoral system?

A

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

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43
Q

What is the most common endpoint for cardiovascular disease?

A

Congestive heart failure

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44
Q

What is diastolic congestive heart failure?

A

Blood does not adequately fill the ventricle causing less blood to pump into circulation

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45
Q

When does diastolic congestive heart failure occur?

A

Ventricles are too thick or stiff

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46
Q

What is systolic congestive heart failure?

A

Inadequate contractile strength to pump an adequate amount of blood out of the heart

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47
Q

When does systolic congestive heart failure occur?

A

Dilated cardiac dysfunction

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48
Q

Which heart failure has decreased ejection fraction?

A

Systolic

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49
Q

What is ejection fraction?

A

Total amount of blood ejected from the heart

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50
Q

Why doesn’t the heart pump well in systolic congestive heart failure?

A

Ischemic injury removes cardiomyocytes
Ventricles are too dilated to pump well (dilated cardiac dysfunction)
Valve regurgitation distends the pump causes it to be ineffective

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51
Q

Which heart failure has normal ejection fraction?

A

Diastolic

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52
Q

What leads to diastolic dysfunction?

A 
HTN
Aortic stenosis
Hypertrophic cardiomyopathy
Fibrosis
Restrictive cardiomyopathy
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53
Q

What can causes myocardial fibrosis?

A

Radiation therapy

Amyloid deposition

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54
Q

What is the pathophysiology of left heart failure?

A

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)

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55
Q

What are the main causes of left heart failure?

A

Myocardial ischemia
HTN
Left-sided valve disease
Myocardial disease

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56
Q

What are the symptoms of left sided heart failure?

A 
Pulmonary congestion/edema
Cough
Dyspnea
SOB
Wheezing
Crackles in lungs
Cough 
Orthopnea (dyspnea when laying flat)
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57
Q

What is paroxysmal nocturnal dyspnea?

A

Dyspnea at night awaking them from sleep

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58
Q

Why does paroxysmal nocturnal dyspnea occur?

A

Respiratory and cough center response is blunted during sleep (feels like they are suffocating)

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59
Q

Impaired left ventricular function in left heart failure can cause what?

A

Atrial dilation leads to atrial fibrillation

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60
Q

Loss of atrial function in atrial dilation and atrial fibrillation leads to what?

A

Pump failure

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61
Q

Lack of perfusion to the brain in left heart failure leads to what?

A

Restlessness
Confusion
Ischemic cerebral injury
Coma

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62
Q

Lack of perfusion to the kidneys in left heart failure leads to what?

A

Azotemia
Increased creatinine
Increased BUN

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63
Q

What edema is seen with left heart failure?

A

Perivascular

Interstital edema

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64
Q

What is seen on CXR with left heart failure?

A

Kerley B lines

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65
Q

What are Kerley B lines?

A

Short parallel lines that reach the lung periphery

Manifestation of interstitial pulmonary edema (specifically interlobular septa)

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66
Q

What other conditions are Kerley B lines seen in?

A

Lymphangitis carcinomatosis
Lymphoma
Pneumonia

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67
Q

What do RBCs do in left heart failure?

A

Extravasate into edema within alveolar spaces

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68
Q

What are the histologic signs of heart failure?

A

Hermosiderin-laden macrophages (due to extravasated RBCs)

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69
Q

What is the most common cause of right heart failure?

A

Left heart failure

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70
Q

Why does left heart failure cause right heart failure?

A

Backpooling of blood from the left heart into the pulmonary vasculature which increases the pressure gradient that the right ventricle has to pump against

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71
Q

Where does the blood pool up in right heart failure?

A

Right atrium

Venous system

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72
Q

What happens to the liver in right heart failure?

A

Impaired hepatic venous draining leading to stasis of blood in the hepatic parenchyma and hepatomegaly

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73
Q

What happens to the spleen in right heart failure?

A

Impaired splenic vein draining

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74
Q

Peritoneal, pleural, and pericardial effusions develop in what type of heart failure?

A

Right heart failure

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75
Q

Why does peritoneal, pleural, and pericardial effusions develop in right heart failure?

A

Intravascular pressure is high, displacing fluid into mesothelial lined body cavities

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76
Q

Marked weight gain is seen in which type of heart failure?

A

Right heart failure

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77
Q

What is the pathophysiology of isolated right sided heart failure?

A

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

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78
Q

What is cor pulmonale?

A

Isolated right-sided heart failure

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79
Q

What are three causes of pulmonary HTN that can leads to isolated right heart failure?

A

1) Parenchymal lung disease
2) Lung thromboemboli
3) Primary pulmonary hypertension

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80
Q

Liver and splenic congestion leads to what in right heart failure?

A

Hepatosplenomegaly

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81
Q

What are the symptoms of right heart failure?

A 
Distended jugular veins
Effusions
Edema (gravity dependent)
Weight gain
Ascites
Fatigue
Exertional dyspnsea
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82
Q

Nutmeg liver is common what type of heart failure?

A

Right sided heart failure

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83
Q

What liver hemorrhage is seen with right sided heart failure?

A

Centrilobular hemorrhage and necrosis

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84
Q

What is emphysema?

A

Chronic pulmonary parenchymal disease

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85
Q

Emphysema causes what cardiac conditions?

A

Pulmonary HTN

Right heart failure

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86
Q

What does the heart look like with cor pulmonale?

A

Hypertrophy of right ventricle

Normal left ventricle

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87
Q

Thromboemboli from DVTs can also cause what type of heart failure?

A

Right heart failure

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88
Q

What is acute cor pulmonale typically attributable to?

A

Large thromboembolus

Multiple thromboemboli in the pulmonary trunk

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89
Q

Thromboemboli in addition to right heart failure causes what?

A

Concomitant decreased systemic and coronary perfusion

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90
Q

What does the majority of congenital heart diseases arise from?

A

Faulty embryogenesis due to sporadic genetic abnormalities

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91
Q

Fetal alcohol syndrome causes what heart defect?

A

Septal defects

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92
Q

What is the most common cardiac abnormality?

A

VSD

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93
Q

What is the most common genetic cause of congenital heart disease?

A

Trisomy 21 (Down Syndrome)

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94
Q

What symptoms do patients with Down Syndrome have?

A 
Epicanthic folds
Flat facial profile
Simian crease
Mental retardation
Abundant neck skin
Intestinal stenosis
Umbilical hernia
Predisposition to leukemia
Hypotonia
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95
Q

What is the most common heart defect with trisomy 21?

A

VSD

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96
Q

What heart defects are common with Marfan syndrome?

A

Aortic aneurysm
Aortic dissection
Mitral valve prolapse
Aortic valve prolapse

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97
Q

DiGeorge syndrome is caused by a deletion in which chromosome?

A

22

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98
Q

What is the CATCH-22 acronym?

A 
Cardiac abnormality
Abnormal facies
Thymic aplasia
Cleft palate
Hypocalcemia
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99
Q

What cardiac abnormality is associated with DiGeorge syndrome?

A

Conotruncal abnormalities

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100
Q

Conotruncal abnormalities occur in which heart field?

A

2nd

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101
Q

What are the conotruncal abnormalities?

A

Tetralogy of fallot

Transposition of great arteries

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102
Q

Turner syndrome is associated with which cardiac abnormality?

A

Coarctation of the aorta

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103
Q

Trisomy 13 (Patau syndrome) is associated with which cardiac abnormalities?

A

PDA

Septal defects

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104
Q

Trisomy 18 (Edward’s syndrome) is associated with which cardiac abnormalities?

A

PDA

Septal defects

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105
Q

What are the two categories of shunts?

A

Left-to-right shunts

Right-to-left shunts

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106
Q

Which side of the heart has higher pressure?

A

Left side

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107
Q

What are the symptoms of left to right shunts?

A

Asymptomatic

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108
Q

What are the symptoms of right to left shunts?

A

Hypoxemia

Cyanosis

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109
Q

What does chronic hypoxemia cause?

A

Polycythemia

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110
Q

What is hypertrophic osteoarthropathy?

A

Inflammation of the periosteum of the connective tissue surrounding bone

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111
Q

What causes hypertrophic osteoarthropathy?

A

Long standing cyanosis

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112
Q

What shunt causing clubbing of tips of finger and toes?

A

Right-to-left

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113
Q

What are the left-to-right shunts?

A

ASD
VSD
PDA

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114
Q

What are the right-to-left shunts?

A 
Tetrology of Fallot
Transposition of the Great Arteries
Tricuspid atresia
Truncus arteriosus
Coarctation of the aorta with PDA
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115
Q

What is the pathophysiology behind hypertrophic osteoarthropathy?

A

Megakaryocyte fragments bypass the lungs and release bradykinin, TGF-Beta1, VEGF, and PDGF causing clubbing, periostitis

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116
Q

All left-to-right shunts cause what?

A

Pulmonary HTN as increased blood increases the pressure in the pulmonary trunk

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117
Q

ASD and VSD causes increase in which volumes?

A

Right ventricles

Pulmonary outflow

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118
Q

PDA causes increase in what volume?

A

Increase pulmonary blood flow

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119
Q

What happens in a paradoxical embolism?

A

Venous embolus crosses to the arterial side (need a defect in the heart or major vessels)

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120
Q

What are the types of emboli?

A

Thromboemboli
Septic emboli
Traumatic bone marrow emboli
Iatrogenic air emboli

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121
Q

What is the most common ASD?

A

Secundum (found in the center of the atrial septum)

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122
Q

What are the symptoms of ASD?

A

Usually asymptomatic (sometimes pulmonary HTN)

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123
Q

How are ASDs fixed?

A

Noninvasive endovascular approach

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124
Q

What are the two other common ASDs?

A 
Primum anomaly (adjacent to AV valves)
Sinus venosa (near entrance to SVC)
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125
Q

What is primum anomaly associated with?

A

AV valve abnormalities

VSD

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126
Q

What is sinus venosa defects associated with?

A

Anomalous pulmonary venous return

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127
Q

What murmur can be seen with ASDs?

A

Ejection systolic murmur

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128
Q

What is the most common congenital cardiac malformation?

A

VSD

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129
Q

Majority of VSDs involve what?

A

Membraneous interventricular septum

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130
Q

What are the other types of VSDs?

A

Subpulmonary (infundibular)
AV canal
Muscular

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131
Q

What are the symptoms of VSDs?

A

Asymptomatic except those associated with tetralogy of fallot

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132
Q

What murmur is seen with VSDs?

A

Holosystolic murmur

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133
Q

Do VSDs close spontaneously?

A

Yes

134
Q

What are the symptoms of large VSDs?

A

Right ventricular hypertrophy
Pulmonary HTN
Shunt reversal -> cyanosis -> death

135
Q

What is the Eisenmenger Syndrome?

A

Shunt reversal in a VSD

136
Q

What pathway for Eisenmenger syndrome?

A

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
Q

Eisenmenger is associated with what?

A

Large VSDs

138
Q

What is the endothelial damage done in Eisenmenger syndrome?

A

Arteriolar intimal proliferation
Medial hypertrophy
Capillary and arteriolar occlusion

139
Q

Is endothelial damage in Eisenmenger syndrome reversible or irreversible?

A

Irreversible

140
Q

What are the two natural shunts in the fetal circulation that bypass the lungs?

A

Foramen ovale

Ductus arteriosus

141
Q

What does the foramen ovale connect?

A

Atria of the heart

142
Q

What keeps the foramen ovale shut after birth?

A

Increased left sided heart pressure

143
Q

What causes the patent foramen ovale to open?

A

Increased right heart pressure
Valsalva
Bowel movement
Coughing/sneezing

144
Q

Opening of a patent foramen ovale causes what?

A

Right-to-left shunting

145
Q

What is clinically significant about a patent foramen ovale?

A

Possible paradoxical embolus

146
Q

What does the ductus arteriosus connect?

A

Pulmonary artery and aorta

147
Q

When does the ductus arteriosus typically close?

A

2-3 days after birth

148
Q

What causes the ductus arteriosus not to close?

A

Hypoxia

Increased vascular pressure

149
Q

What murmur is heard with patent ductus arteriosus?

A

Harsh, continuous medium pitched murmur with machine-like quality

150
Q

What is used to close a patent ductus arteriosus?

A

Indomethacin

151
Q

What shunt occurs with patent ductus arteriosus?

A

Left-to-Right

152
Q

What can happen with a large patent ductus arteriosus?

A

Increased pulmonary pressure

Shunt reversal -> Cyanosis

153
Q

What is used to preserve the patency of ductus arteriosus in certain congenital malformation?

A

Prostaglandin E

154
Q

What are the four features of tetralogy of fallot?

A

1) VSD
2) Right ventricular hypertrophy
3) Pulmonary valve stenosis
4) Overriding aorta

155
Q

What is an overriding aorta?

A

Entrance to the aorta is centered at the VSD instead of the main part of the left ventricle

156
Q

What causes the right ventricular hypertrophy in tetralogy of fallot?

A

Pressure overload induced by pulmonary stenosis

157
Q

What dictates the clinical severity of Tetralogy of Fallot?

A

Degree of pulmonary stenosis

158
Q

What is the most common cyanotic congenital heart disease?

A

Tetralogy of Fallot

159
Q

What murmur is heard with tetralogy of fallot?

A

Holosystolic murmur and/or systolic ejection murmur

160
Q

What does the holosystolic murmur depend on in tetralogy of fallot?

A

Degree of VSD

161
Q

What does the systolic ejection murmur depend on in tetralogy of fallot?

A

Degree of pulmonary stenosis

162
Q

Infants with what in tetralogy of fallot require immediate intervention?

A

Severe pulmonary stenosis

163
Q

Is right ventricular outflow tract or pulmonic valve stenosis progressive in tetralogy of fallot?

A

Yes

164
Q

What are “tet” spells

A

Significant obstruction of the pulmonary outflow tract triggered by increased demand such as during period of excitement, crying, feeding, or increased activity

165
Q

What are the symptoms of “tet” spells?

A

Cyanosis

Syncope

166
Q

Why do children squat during “tet” spells?

A

Increases peripheral vascular resistance which decreases the degree of right to left shunting (allows them to oxygenate better)

167
Q

Does clubbing of the fingers occur with tetralogy of fallot?

A

Yes

168
Q

What is seen on x-ray in a patient with tetralogy of fallot?

A

Boot shaped heart

169
Q

What causes the boot shaped heart seen with tetralogy of fallot?

A

Upturned cardiac apex caused by right ventricular hypertrophy and a concave pulmonary arterial segment

170
Q

What happens in the classic form of transposition of the great arteries?

A

Right ventricle is connected to the aorta

Left ventricle is connected to the pulmonary trunk

171
Q

Is transposition of the great arteries compatible with life?

A

No

172
Q

What is often kept open if a baby is born with transposition of the great arteries?

A

Ductus arteriosus with prostaglandin E1

173
Q

Transposition of the great vessels results in what type of shunt?

A

Right-to-left

174
Q

Which ventricle hypertrophies in the transposition of the great arteries?

A

Right ventricle

175
Q

What are the symptoms associated with transposition of the great vessels?

A

Cyanosis

Trouble breathing

176
Q

What is tricuspid atresia?

A

Absence of the tricuspid valve

177
Q

Is tricuspid atresia compatible with life?

A

No (not without ASD or VSD)

178
Q

What is the left ventricle responsible for in transposition of the great vessels?

A

Pumping blood to both the right ventricle, lungs, and systemic circulation

179
Q

What is needed immediately after birth for tricuspid atresia?

A

Surgical correction

180
Q

What is coarctation of the aorta?

A

Obstructive defect which manifests as focal narrowing of the aorta

181
Q

Which gender is coarctation of the aorta most common in?

A

Males

182
Q

If females are seen with coarctation of the aorta what syndrome should be suspected?

A

Turner’s syndrome

183
Q

What is associated with half of the cases of coarctation of the aorta?

A

Bicuspid aortic valve

184
Q

Patients with coarctation of the aorta have an increased risk of what?

A

Berry aneurysm which predisposes them to intracerebral hemorrhage

185
Q

Infantile coarctation of the aorta is characterized by what?

A

Preductal coarctation (located before the ductus arteriosus) -> significantly less blood flow to the lower half of the body

186
Q

Adult coarctation of the aorta is characterized by what?

A

Coarctation at the ductal arteriosus or in a postductal location

187
Q

Diminished pulses is seen in which form of coarctation of the aorta?

A

Adult

188
Q

Is there cyanosis with coarctation of the aorta?

A

Yes

189
Q

What is seen on CXR with adult coarctation of the aorta?

A

Tortuous collateral intercostal vessels which cause pressure erosion of the inferior rib margins causing rib notching

190
Q

What is the difference between the infantile and adult form of coarctation of the aorta?

A

Infantile form has a PDA

Adult for does NOT have a PDA

191
Q

What does the clinical presentation of coarctation of the aorta depend on?

A

Severity of stenosis

192
Q

What are the symptoms of the infantile form of coarctation of the aorta?

A 
Cyanosis in lower extremities
Absent lower extremity pulses
Heart failure
Shock
Pale, irritable, diaphoretic, SOB
193
Q

What are the symptoms of coarctation of the aorta without PDA?

A 
Hypertension in upper extremities
Hypotension in lower extremities
Cold lower extremities
Femoral artery pulse delay
Pain in extremities with exercise
194
Q

What hypertrophy is seen with coarctation of the aorta?

A

Concentric left ventricular hypertrophy (also heart failure)

195
Q

Which valve dysfunctions can be see with aortic stenosis?

A

Hypoplastic (small)
Dysplastic (nodular thickened)
Abnormal cusp number

196
Q

What hypertrophy is seen with aortic stenosis?

A

Concentric left ventricular hypertrophy (due to pressure overload)

197
Q

What is hypoplastic left heart syndrome?

A

Aorta is stenotic or atretic and oxygenated blood flow is only possible through an atrial septal defect with a PDA

198
Q

What is the blood flow in hypoplastic left heart syndrome?

A

Right ventricle -> lungs -> left atrium -> right heart (through ASD) -> right ventricle pumps blood to systemic (through PDA)

199
Q

What hypertrophy is seen with pulmonary stenosis?

A

Right ventricular hypertrophy

200
Q

What two complexes is pulmonary stenosis associated with?

A

Tetralogy of Fallot

Transposition of the Great Arteries

201
Q

What are the causes of ischemic heart disease?

A

Atherosclerosis
Coronary artery emboli
Myocardial vessel inflammation (vasculitis)
Vessel spasm

202
Q

What are the classic clinical features of myocardial infarction?

A 
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
Q

Nausea and vomiting are related to what specific MI location?

A

Posterior-inferior (due to vagal stimulation)

204
Q

Diabetic neuropathy may hide symptoms of what?

A

Myocardial infarction

205
Q

How is myocardial infarction diagnosed?

A 
Symptoms
EKG changes
Cardiac markers (troponin)
206
Q

Myocardial ischemia leads to loss of function after how many minutes?

A

1-2 minutes

207
Q

Necrosis occurs how long after myocardial infarction?

A

20-40 minutes

208
Q

How long after a MI is neurologic recovery unlikely?

A

5-7 minutes

209
Q

How long after a MI is severe irreversible brain damage probable?

A

10 minutes

210
Q

What is cardioplegia?

A

Heart is cooled significantly lowering the myocytes metabolic rate and preventing ischemic death

211
Q

Oxygen consumption of myocytes drops 50% for every how much reduction in temperature?

A

10 degrees celsius

212
Q

After MI how long before onset fo ATP depletion?

A

Seconds

213
Q

After MI how long before loss of contractility?

A

Less than 2 minutes

214
Q

After MI how long before ATP reduced to 50% of normal?

A

10 minutes

215
Q

After MI how long before ATP is reduced to 10% of normal?

A

40 minutes

216
Q

After MI how long before irreversible cell injury?

A

20-40 minutes

217
Q

After MI how long before microvascular injury?

A

1 hour

218
Q

What are the most specific and sensitive markers we have for acute myocardial infarction?

A

Troponin T

Troponin I

219
Q

What are the function of troponin T and I?

A

Regulate calcium mediated contraction of cardiac muscle

220
Q

Which troponin is currently used by most labs?

A

Troponin I

221
Q

Which creatine kinase isoform is present in cardiac muscle?

A

MB heterodimer

222
Q

Which creatine kinase isoform is present in muscle?

A

MM

223
Q

What creatine kinase isoform is present in the brain and lung?

A

BB

224
Q

Is CK-MB sensitive?

A

Yes

225
Q

Is CK-MB specific?

A

No

226
Q

What is released by cardiac muscle with injury but is nonspecific?

A

Myoblobin

227
Q

Are troponin I and T normally detected in circulation?

A

No

228
Q

What releases troponin I and T

A

Dead and dying cardiomyocytes

229
Q

When does dying cardiomyocytes start releasing troponin?

A

3 hours

230
Q

Why are serial troponin draws necessary?

A

Patient could have a heart attack prior to an increase in troponin levels

231
Q

When does CK-MB go back to baseline?

A

48-72 hours after infarction

232
Q

How long is troponin elevated for?

A

5 days

233
Q

CK-MB is specifically utilized to assess for what?

A

Reinfarction of the heart after initial heart attack

234
Q

When does CK-MB and troponin I peak?

A

24 hours

235
Q

What arteries are most commonly occluded in MI?

A

LAD > right coronary artery > left circumflex artery

236
Q

Occlusion of the LAD causes infarction of what?

A

Apex
LV anterior wall
Posterior 2/3 of septum

237
Q

Occlusion of the left circumflex artery causes infarction of what?

A

LV lateral wall

238
Q

Occlusion of the right coronary artery causes infarction of what?

A

RV free wall
LV posterior wall
Posterior 1/2 of septum

239
Q

When does a subendothelial infarct occur?

A 
Reperfusion of transmural infarct (regional)
Global hypotension (circumferential)
240
Q

What happens with a reperfusion of transmural infarct?

A

Blocking thrombus is dislodge either spontaneously or through thrombolytic therapy -> regional subendocardial infarct

241
Q

When does global hypotension occur?

A

Shock/significant coronary artery stenosis -> circumferential subendocardial infarct

242
Q

What is a multifocal microinfarction?

A

Numerous small infarcts occur within the smaller intramural vessels of the myocardium

243
Q

What causes a multifocal microinfarction?

A

Cocaine use

Embolic disease

244
Q

How do coronary artery perfuse the heart muscle?

A

Epicardium -> endocardium

245
Q

What is the last portion of the heart to get perfused?

A

Myocardium near the endocardial surface

246
Q

How do infarctions spread?

A

Inside of the heart out (necrotic core expands into the overlying tissue)

247
Q

What perfuses the endocardium?

A

Blood in the heart chamber (this portion of the heart still viable despite the infarction)

248
Q

What does the rate of necrosis throughout the heart depend on with a MI?

A

Degrees of collateral circulation with areas being fed by a single vessel taking a shorter time to become a transmural infarct

249
Q

What is seen on the electron microscope at 0 hours?

A

Relaxation of myofibrils
Glycogen loss
Mitochondrial swelling

250
Q

What is seen on light microscope from 0.5-4 hours?

A

Waviness of fibers at border (due to sarcolemmal disruption)

251
Q

What is seen on electron microscope from 0.5-4 hours?

A

Sarcolemmal disruption

Mitochondrial amorphous densities

252
Q

What is seen grossly from 4-12 hours

A

Dark mottling

253
Q

What is seen on light microscope from 4-12 hours?

A

Early coagulation necrosis
Edema
Hemorrhage

254
Q

What is seen grossly from 12-24 hours?

A

Dark mottling

255
Q

What is seen on light microscope from 12-24 hours

A 
Ongoing coagulative necrosis
Pyknosis of nuclei
Myocyte hypereosinophila
Marginal contraction band necrosis
Early neurtrophilic infiltrate
256
Q

What is pyknosis?

A

Condensation of the chromatin in the nucleus

257
Q

What is seen grossly from 1-3 days?

A

Mottling with yellow-tan infarct center

258
Q

What is seen on light microscope from 1-3 days?

A

Coagulation necrosis
Loss of nuclei and striations
Brisk interstital infiltrate of neutrophils

259
Q

What is seen grossly from 3-7 days?

A

Hyperemic border

Central yellow-tan softening

260
Q

What is seen on light microscope from 3-7 days?

A

Beginning disintegration of dead myofibers with dying neutrophils
Early phagocytosis of dead cells by macrophages at infarct border

261
Q

What is seen grossly from 7-10 days?

A

Maximally yellow tan, and soft, with depressed red-tan margins

262
Q

What is seen on light microscope from 7-10 days?

A

Well-developed phagocytosis of dead cells

Granulation tissue at margins

263
Q

What is seen grossly from 10-14 days?

A

Red-gray depressed infarct borders

264
Q

What is seen on light microscope from 10-14 days?

A

Well-established granulation tissue with new blood vessels and collagen deposition

265
Q

What is seen grossly from 2-8 weeks?

A

Gray-white scar, progressive from border towards core of infarct

266
Q

What is seen on light microscope from 2-8 weeks?

A

Increased collagen deposition

Decreased cellularity

267
Q

What is seen grossly from 2 months?

A

Scarring complete

268
Q

What is seen on light microscope from 2 months?

A

Dense collagenous scar

269
Q

What is the first sign of irreversible injury in myocardial infarction?

A

Wavy fiber change

270
Q

What causes the wavy fiber change after MI?

A

Mechanical pulling by viable fibers on dead fibers resulting in folding and twisting

271
Q

What leaks out of dead myoctyes after 2-3 hours

A

Lactate dehydrogenase

272
Q

What stain is used to identify lactate dehydrogenase after MI?

A

Triphenyltetrazolium chloride

273
Q

Do areas of infarction hemorrhage or scar turn bright red with the triphenyltetrazolium choloride?

A

No

274
Q

What happens cellularly with irreversible injury to myocytes?

A

Cell membrane disrupted with reperfusion
Influx of calcium causing sarcomeres to contract
Contraction bands on light microscopy (contraction band necrosis)

275
Q

What replaces normal myocytes after MI?

A

Fibroblasts with increased collagen

276
Q

What are early complications of MI?

A 
Life threatening arrhythmia (v tach, v fib)
Contractile dysfunction (shock)
277
Q

What are intermediate complications of MI?

A

Rupture: septal, wall, papillary

Acute pericarditis

278
Q

What are the late complications of MI?

A 
Chronic pericarditis (Dressler syndrome)
Ventricular aneurysm (remodeling)
Continued risk of heart failure, life threatening arrhythmia
279
Q

What causes mitral regurgitation after MI?

A

Ischemic papillary muscles

280
Q

What is the most common mechanical complication of MI?

A

Papillary muscle rupture

281
Q

Which infarct causes papillary muscle rupture?

A

Right circumflex artery

282
Q

Which infarct causes ventricular septal rupture?

A

Anterior infarcts

283
Q

What is the most common cause of death due to MI?

A

Fatal arrhythmias (v fib)

284
Q

What is the second most common cause of death after MI?

A

Cardiogenic shock (pump failure due to contractile dysfunction due to the death of heart muscle)

285
Q

When does myocaridal rupture typically occur after MI?

A

2-4 days

286
Q

Myocardial rupture after MI requires what?

A

Transmural infarct

287
Q

Rupture of the free wall can lead to what?

A

Blood accumulating in the pericardial space

288
Q

What is blood accumulating in the pericardial space called?

A

Acute pericardial tamponade

289
Q

What happens to the heart during acute pericardial tamponade?

A

Heart is unable to adequately fill during diastole because of the pressure of the blood in the pericardial sac

290
Q

Septal rupture can lead to what?

A

VSD with left to right shunting

291
Q

Papillary muscle rupture can lead to what?

A

Valve incompetence

Post infarct regurgitation

292
Q

Why does myocardial rupture occur more often in the elderly?

A

Lower muscle mass

293
Q

What is pericarditis?

A

Inflammation of the pericardium

294
Q

What is present with acute pericarditis?

A

Pericardial friction rub

295
Q

When does myocardial rupture and acute pericarditis occur post MI?

A

2-4 days

296
Q

What are the risk factors for myocardial rupture?

A

Increased age
First MI
Absence of LV hypertrophy

297
Q

Acute pericardial tamponade leads to what?

A

Hemodynamic collapse

298
Q

When do late complications of MI occur?

A

After 2 weeks

299
Q

What is Dressler syndrome?

A

Fibrinous pericarditis

300
Q

What causes Dressler syndrome?

A

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
Q

What is the end result of Dressler syndrome?

A

Febrile pericarditis
Pericardial effusion
Pleuritic pain

302
Q

What causes the late complication of ventricular aneurysm post MI?

A

Thin scarred ventricular wall

303
Q

What causes progressive heart failure after MI?

A

Inadequate compensatory response

304
Q

What is seen grossly with Dressler syndrome?

A

Dark, roughened epicardial surface

305
Q

What is the definition of angina pectoris?

A

Transient, often recurrent chest pain induced by myocardial ischemia insufficient to induce myocardial infarction

306
Q

What are the three types of angina pectoris?

A

1) Stable angina
2) Prinzmetal variant angina
3) Unstable angina

307
Q

What is released due to lack of oxygen in the heart muscle?

A

Adenosine

Bradykinin

308
Q

Which patients often have silent angina?

A

Elderly
Previous MI
Diabetic neuropathy

309
Q

What is stable angina?

A

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
Q

What causes stable angina?

A

Stenotic occlusion of coronary artery

311
Q

What are the symptoms of stable angina?

A

Substernal pressure, squeezing, burning

312
Q

What relieves stable angina?

A

Rest

Vasodilators

313
Q

What induces stable angina?

A

Physical activity

Stress

314
Q

What is prinzmetal variant angina?

A

Episodic coronary artery spasm

315
Q

What makes prinzmetal variant angina worse?

A

Aterosclerotic disease

316
Q

When does prinzmetal variant angina occur?

A

At rest

317
Q

Is prinzmetal variant angina associated with physical activity?

A

No

318
Q

What is the pattern of prinzmetal variant angina?

A

3-6 month clusters of recurrent attacks separated by asymptomatic periods

319
Q

What is given to to alleviate the symptoms of prinzmetal variant angina?

A

Vasodilators (nitrate)

320
Q

What is unstable angina?

A

Angina which is present at rest or angina that increases in frequency or duration

321
Q

What is the most common cause of unstable angina with acute chest pain with activity and rest?

A

Rupture of atherosclerotic plaque which results in a non-occlusive thrombus

322
Q

What causes unstable progresive angina?

A

Progressive obstruction

323
Q

What type of pattern is there with unstable angina?

A

Crescendo patern

324
Q

When is table angina symptomatic?

A

Only with increased demand for oxygen during exercise or activity

325
Q

Unstable angina is due to what?

A

Problem with overall supply of oxygen even at rest

326
Q

ST elevation on EKG corresponds with what?

A

Transmural infarction

327
Q

When there isn’t a ST elevation on EKG what is on the differential?

A

NSTEMI

Unstable angina

328
Q

What can be used to tell the difference between NSTEMI and unstable angina?

A

Presence of troponin

329
Q

Is troponin elevated in NSTEMI?

A

Yes

330
Q

Is troponin elevated in unstable angina?

A

No

331
Q

Does unstable angina or NSTEMI show ST elevations?

A

No

CPR 2 Exam 1 (20 decks)

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