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CPR Exam 1 > Heart Pt. 1 > Flashcards

Heart Pt. 1 Flashcards

1
Q

What is hypertrophy?

A

increase in ventricular thickness

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2
Q

What is heart dilation?

A

enlarged chanber size

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3
Q

What is cardiomegaly?

A

increase in cardiac wt

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4
Q

What does Atrial Natriuretic Peptide do?

A

stimulates renal salt and water elimination (natriuresis and diuresis)
* beneficial in setting with HTN and CHF!

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5
Q

What are the 3 types of cardiac damage mentioned, and give their example

A
  1. collagen: mitral prolapse
  2. nodular calcification: calcific aortic stenosis
  3. fibrotic thickening: rheumatic heart dz
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6
Q

What starts ventricular diastole?

A

closing of the aortic valve, leading to blood flow to myocardium thru coronary vessels

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7
Q

What is lipofiscin?

A

wear and tear on heart leaves yellow/brown lipid deposits in the myocardium

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8
Q

What is the danger with mitral valve calcification?

A

it can affect electrical signaling

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9
Q

What are Llambl excrescences?

A

small filliform processes that form on the closure lies of the aortic and mitral valves, most likely resulting from the organization of small thrombi

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10
Q

What is basophilic degeneration?

A

pathologic blue staining of connective tissue on H&E stain

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11
Q

What is pump failure?

A
  • weak myocardium contraction during systole leads to inadequate CO
  • myocardium may relax insufficiently during diastole to permit adequate ventricular filling
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12
Q

What is flow obstruction?

A

lesions obstructing blood flow through a vessel (atherosclerotic plaque) that prevent valve opening, or cause increased ventricular chamber pressure

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13
Q

What is regurgitant flow?

A

portion of the output from each contraction flows backward through an incompetent valve, adding volume overload to the affected atria or ventricles

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14
Q

What is shunted flow?

A

blood can be diverted from one part of the heart to another thru defects that can be congenital or acquired

NOTE: can also occur between blood vessels

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15
Q

What is cardiac exsanguination?

A

the loss of enough blood to cause cardiac death

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16
Q

When does CHF occur?

A

when the heart is unable to pump blood at a rate to meet peripheral demand, or can only do so with increased filling pressure

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17
Q

What causes CHF?

A

may result from

  • loss of contractile function (systolic dysfunction)
  • loss of ability to fill the ventricles during diastole
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18
Q

What causes cardiac myocytes to become hypertrophic?

A
  1. sustained pressure or volume overload (systemic HTN or aortic stenosis)
  2. sustained trophic signals (beta-adrenergic stimulation)
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19
Q

What does pressure overload hypertrophy lead to?

A

myocytes become thicker, LV increases in thickness concentrically

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20
Q

What does volume over load hypertrophy lead to?

A

myocytes elongate and ventricular dilation seen

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21
Q

What is the best way to measure cardiac hypertrophy?

A

heart weight (rather than wall thickness)

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22
Q

Why the the hypertrophied heart vulnerable to ischemia-related decompensation?

A

because myocyte hypertrophy is NOT accompanied by a matching increase in blood supply, despite the increase in energy demand

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23
Q

What are the 4 most common causes of left-sided heart failure?

A
  1. myocardial ischemia
  2. HTN
  3. left-sided valve disease
  4. primary myocardial disease
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24
Q

What causes clinical effects of left-sided heart failure?

A
  • pulmonary circulation congestion

- decrease in tissue perfusion

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25
Q

What are the symptoms of pulmonary congestion?

A
  • cough
  • crackles
  • wheezes
  • blood-tinged sputum
  • tachypnea
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26
Q

What is the histological hallmark of left-sided heart failure?

A

heart failure cells! aka hemosiderin-laden macrophages

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27
Q

What does left ventricular dysfunction lead to?

A

left atrial dilation, which can cause atrial fibrillation, stasis, or thrombus

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28
Q

What does decreased ejection fraction lead to?

A

decreased glomerular perfusion

- stimulates renin release -> increased fluid volume

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29
Q

What is prerenal azotemia?

A

aka prerenal failure

- when excess nitrogen compounds in the blood due to lack of blood flow to the kidneys

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30
Q

What can advanced CHF lead to?

A

decreased cerebral perfusion (hypoxic encephalopathy)

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31
Q

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

A

LEFT-SIDED HEART FAILURE

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32
Q

What are the 3 main causes of isolated right sided-heart failure?

A
  1. parenchymal lung disease
  2. primary pulmonary HTN
  3. pulmonary vasoconstriction
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33
Q

What is congested in primary right-sided failure?

A

the venous system!

- pulmonary congestion is minimal

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34
Q

What is seen in primary right-sided failure?

A
  • nutmeg liver
  • splenic congestion -> splenomegaly
  • peritoneal, pleural and pericardial effusions
  • peripheral edema
  • renal congestion
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35
Q

When do you see congestion of venous circulation?

A

when there is inadequate cardiac output (CHF)

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36
Q

What is the most common cause of left-sided heart failure?

A

ischemic heart disease, systemic HTN, mitral or aortic valve disease, and primary diseases of the myocardium

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37
Q

What are the symptoms of right heart failure related to?

A

peripheral edema and visceral congestion

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38
Q

What are the major known causes of congenital heart disease?

A

sporadic genetic abnormalities!

- Turner syndrome, trisomies 13, 18, 21

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39
Q

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

A

trisomy 21**- 40% of Down syndrome pts have at least one heart defect

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40
Q

What are the most common heart defects in Trisomy 21?

A

defects of the endocardial cushion

- ostium primum, ASDs, AV valve malformations, VSDs

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41
Q

What is the Notch pathway associated with?

A

a variety of congenital heart defects, including bicuspid aortic valve (NOTCH1) and tetralogy of Fallot (JAG1 and NOTCH2)

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42
Q

What are Fibrillin mutations associated with?

A

valvular defects and aortic aneurysms

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43
Q

What is the most common congenital cardiac malformation?

A

ventricular septal defect (90%)

44
Q

What causes CHARGE syndrome? What are the effects?

A

helicase-binding protein defect (CHD7 gene)

- ASD, VSD, PDA, hypoplastic right side of the heart

45
Q

What causes DiGeorge syndrome? What are the effects?

A

transcription factor defect (TBX1 gene)

- ASD, VSD, or outflow tract obstruction

46
Q

What are the common congenital left-to-right shunts?

A

ASD: increases RV and pulmonary outflow volumes

VSD, PDA: increase pulmonary blood flow and pressure

47
Q

Which type of heart defect can go unnoticed until adulthood?

A

atrial septal defect

48
Q

What is secundum ASD?

A

90% of all ASDs, center of atrial septum, may be multiple or fenestrated

49
Q

What is primum anomalie?

A

5% of all ASDs, near entrance of SVD (single ventricle defect), can be associated with anomalous pulmonary venous return to the R atrium

50
Q

What is TAPVR?

A

total anomalous pulmonary venous return

  • rare congenital malformation in which all four pulmonary veins do not connect normally to the left atrium
  • instead the four pulmonary veins drain abnormally to the right atrium
51
Q

What does left-to-right shunting cause? What does it lead to?

A

volume overload on the right side, which may lead to

  • pulmonary HTN
  • right heart failure
  • paradoxical embolization (patent foramen ovale)
52
Q

What will an increase in right sided pressure do to a PFO?

A

the flap can open, producing brief periods of R-L shunting, which can lead to a paradoxical embolus

53
Q

What is an infundibular VSD?

A

below the pulmonary valve, within muscular septum

54
Q

What can large VSDs lead to?

A
  • right ventricular hypertrophy
  • pulmonary HTN
  • unclosed large VSD can ultimately result in shunt reversal, leading to cyanosis and death
55
Q

What kind of murmur does a PDA produce?

A

harsh, machinery-like murmur

  • usually asymptomatic at birth
  • initially left-to-right, so NO CYANOSIS
56
Q

What can saving in infants with obstruction of pulmonary or systemic outflow?

A

Prostaglandin E

57
Q

What is the most common Right-to-Left shunt? Other examples?

A
  • *Tetralogy of Fallot**
  • transposition of the great arteries
  • persistent truncus arteriosus
  • tricuspid atresia
  • total anomalous pulmonary venous connection

NOTE: q’s often mention third world country, because these shunts are repaired very early in US

58
Q

What type of shunt causes cyanosis in early postnatal life?

A

right-to-left shunts

59
Q

What are the four cardinal features of Tetralogy of Fallot?

A
  1. VSD
  2. obstruction of RV outflow tract
  3. aorta overrides VSD
  4. RV hypertrophy
60
Q

When would you see an enlarged, “boot-shaped” heart?

A

Tetralogy of Fallot

- because RV hypertrophy

61
Q

What is the classic presentation of Tetralogy of Fallot?

A

right-to-left shunting with cyanosis***

- most infants cyanotic from birth

62
Q

What does Transposition of the great vessels (TGA) result in?

A

two separate systemic and pulmonary circulations

  • incompatible with life after birth unless a shunt is present (mixing blood from the two circulations)
  • 1/3 have a VSD
  • 2/3 have PDA or PFO
  • RV becomes hypertrophic, LV atrophies
63
Q

What does Coarctation of the Aorta cause?

A

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

64
Q

When do you see coarctation of the aorta?

A

2x males > females, TURNER SYNDROME**

65
Q

What causes cyanosis in the lower half of the body?

A

coarctation of the aorta with PDA, manifests at birth

66
Q

What are the symptoms of coarctation without PDA?

A

usually asymptomatic at brith…

  • HTN in upper extremities, hypotension in lower extremities
  • claudication and cold LE***
  • may eventually see concentric LV hypertrophy
  • enlarged mammary arteries “notching” on undersurface of ribs
67
Q

What is Eisenmenger syndrome?

A

VSD causes increased blood flow to pulmonary arteries
- eventually pressure in pulmonary arteries becomes so high that it causes oxygen-poor blood to flow from right to left ventricles

68
Q

What does ischemic heart disease result from?

A

insufficient perfusion to meet metabolic demands of the myocardium

69
Q

What can ischemic heart disease lead to?

A
  • MI
  • angina pectoris
  • chronic ischemic heart disease, with heart failure
  • sudden cardiac death
70
Q

What is the leading cause of death in the US? What are 90% of cases secondary to?

A

ischemic heart disease

- atherosclerosis (chronic vascular occlusion, thrombus)

71
Q

What is angina pectoris?

A

transient, often recurrent chest pain induced by myocardial ischemia

72
Q

What are the 3 clinical variants of angina?

A
  1. stable angina
  2. prinzmetal “variant” angina
  3. unstable “crescendo” angina
73
Q

What is stable angina?

A

stenotic occlusion of coronary artery

  • “squeezing” or burning sensation, releived by rest of vasodilators
  • induced by physical activity, stress
74
Q

What is prinzmetal “variant” angina?

A

episodic coronary artery spasm, relieved with vasodilators

- unrelated to physical activity, HR or BP

75
Q

What is unstable “crescendo” angina?

A

pain that increases in frequency, duration and severity, at progressively lower levels of physical activity, eventually even at rest

  • usually caused by a rupture of atherosclerotic plaque, with partial thrombus
  • 50% may have evidence of myocardial necrosis, acute MI may be imminent**
76
Q

What causes 90% of myocardial infarctions? What are other causes?

A

atheromatous plaques**

  • embolus
  • vasospasm
  • ischemia secondary to vasculitis, shock, hematologic abnormalities
77
Q

What is the classic presentation of an MI?

A

in men: prolonged chest pain (>30mins)

  • crushing, stabbing, squeezing, tightness
  • radiating down left arm or left jaw
  • diaphoresis*
  • dyspnea
  • nausea, vomiting
78
Q

What is the timeline of irreversible cell injury following MI?

A

20-40 mins

79
Q

What is the timeline of microvascular injury following MI?

A

> 1 hr

80
Q

What are the major coronary arteries affected by MI?

A
  • LAD (40-50%)
  • RCA (30-40%)
  • L circumflex (15-20%)
81
Q

What areas of the heart would an occlusion of LAD affect?

A

apex, LV anterior wall, anterior two thirds of septum

82
Q

What areas of the heart would an occlusion of RCA affect?

A

RV free wall, LV posterior wall, posterior two thirds of septum

83
Q

What area of the heart would an occlusion of L circumflex artery affect?

A

LV lateral wall

84
Q

What do you see 4-12 hours after irreversible cardiac injury?

A

early coagulation necrosis, edema, hemorrhage

85
Q

What do you see 12-24 hours after irreversible cardiac injury?

A
  • dark mottling
  • myocyte hypereosinophilia**
  • contraction band necrosis
  • early neutrophilic infiltrate**
86
Q

What do you see 7-10 days after irreversible cardiac injury?

A

maximally yellow-tan and soft tissue, with depressed red-tan margins

  • well developed phagocytosis of dead cells
  • granulation tissue at margins
87
Q

What do you see 3-7 days after irreversible cardiac injury?

A

hyperemic border, central yellow-tan softening

- dying neutrophils, early phagocytosis of dead cells by macrophages** at infarct border

88
Q

What do you see 10-14 days after irreversible cardiac injury?

A

red-gray depressed infarct borders

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

89
Q

What do you see 24 hours after acute MI?

A
  • coagulative necrosis
  • pyknotic nuclei
  • loss of cross striations
90
Q

What do you see 1-3 days post MI?

A
  • loss of striations

- neutrophilic infiltration

91
Q

What is granulation tissue considered?

A

part of the healing process

92
Q

What is reperfusion?

A

restoring blood flow to an area of ischemia and impending infarction
- an attempt to limit the infarct size by rescuing at risk myocardium

93
Q

What is seen histologically in a reperfusion injury?

A
  • contraction bands
  • loss of striations
  • different coloration
94
Q

What is the first mycoyte protein to peak following MI?

A

myoglobin (peaks 4-6 hours after injury)

- levels drop quickly after peak

95
Q

What is the second myocyte protein to peak following MI?

A

CK-MB (peaks 16-20 hours after injury)

- not as specific

96
Q

When do Troponin levels peak following MI?

A

approx 24 hours post MI

97
Q

What are the most useful myocyte proteins to measure post MI?

A

Troponin T and Troponin I (cTnT, cTnI)

98
Q

What are the most sensitive and specific biomarkers of myocardial damage? Why

A

cTnT and cTnI

- because they are not normally detectable in circulation

99
Q

When do troponin levels begin to rise post MI?

A

3-12 hours

100
Q

When do cTnT and cTnI levels peak?

A

cTnT: 12-48 hours
cTnI: maximal at 24 hours

101
Q

Why is creatine kinase-MB (CK-MB) sensitive, but not specific to MIs?

A

MB heterodimers are found in skeletal muscle as well as cardiac muscle, so they can be elevated after skeletal muscle injury

102
Q

When do CK-MB levels rise?

A

they begin to rise within 3-12 hours post MI, peak at 24 hours, and return to normal within 48-72 hours

103
Q

What is the most common complication from an MI?

A

arrhythmias

- half of all MI deaths occur within 1 hour of onset, usually secondary to an arrhythmia

104
Q

What causes an arrhythmia?

A

they can result from permanent damage to the conducting system, or from myocardial “irritability”

105
Q

What are other complications of an MI?

A
  • contractile dysfunction (depends on size of infarct and associated loss of function)
  • fibrinous pericarditis (bread and butter pericarditis)
106
Q

What is myocardial rupture? What are the risk factors?

A
  • typically required a transmural infarct
  • 2-4 days post MI, when inflammation and necrosis have weakened the wall

Risk factors: age, large transmural anterior MI, absence of LV hypertrophy

107
Q

What is a ventricular aneurysm?

A
  • late complication of large transmural infarct with early expansion
  • composed of thinned/scarred myocardium
  • also associated with mural thrombus (that attach to wall of chamber)

CPR Exam 1 (18 decks)

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